Fargette, Denis

Fauquet, Claude

Horizon / Pleins textes

Aspects of Applied Biology 17, 1988 
Environmental aspects of applied biology 
A preliminary study on the influence of intercropping maize and cassava on 
the spread of African cassava mosaic virus by whiteflies 
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. D. FARGETTE and C.  FAUQUET 
Laboratoire de Virologie, Institut Français de Recherche pour le Développement en Coopération 
(ORSTOM). BP V51 Abidjan, Côte d'Ivoire. 
SUMMARY 
Spread of African cassava mosaic virus (ACMV) in mixed crops of cassava with 
maize was different from that in a cassava monoculture. Not only the temporal but 
also the spatial pattern of disease spread and the dynamics of the vector were 
modified. The effects of mixed cropping on ACMV incidence were complex and 
cannot be due simply to protection of the cassava by the taller maize against 
incoming whitefly vectors. Moreover, the maize, whatever its height, did not 
always reduce the incidence of ACMV and greater incidences occurred in some 
maize/cassava combinations compared with the monoculture. The practical 
implication of the results is that caution is necessary in drawing conclusions from 
experimental trials carried out exclusively in  monoculture as it could lead to 
incorrect advice being given to farmers who usually plant mixed stands. 
INTRODUCTION 
African cassava mosaic virus (ACMV) is disseminated in cuttings and transmitted by the 
whitefly Bemisia tabaci in a persistent manner. Yield losses induced by the disease range from 
20 to 95% according to the variety tested, time of infection and conditions of growth (Guthrie, 
1988; Fargette, Fauquet & Thouvenel, 1988). Two main strategies of control are being 
developed. Resistance breeding programmes against ACMV have continued since 1934 
(Jennings, 1988). Alternatively, in areas where spread by whitefly is restricted, planting 
uninfected cuttings and subsequent roguing of further infections have enabled virtually healthy 
cassava stands to be maintained, for example, in various parts of Kenya (Bock, 1983). This 
strategy has also been applied sucessfully at a site in the savannah region of the Ivory Coast 
-(Fauquet, Fargette and Thouvenel, 1988). Promising results have aEso been obtained in the 
forest region provided that a suitably resistant variety is used (Fargette & Fauquet, unpublished 
results). 
The main requirement for determining if this strategy is feasible is a knowledge of the overall 
'inoculum pressure'. Thus, for each area, the inoculum pressure has to be determined 
experimentally by assessing rates of recontamination. So far, all experiments on rates of 
contamination,. either-on-experimental stations o? in peasant farms, have been conducted in 
monocultures of cassava. These $e atypical because cassava is usually grown in Africa in 
association with other crops in Farious spatio/temporal combinatipns and arrangement,s 1 
(Sylvestre & Arraudeau, 1983). Few studies have been conducted on the effect of mixed 
cropping on the spread of vector-borne viruses, although many tropical crops are cultivated in 
this way. However, the few examples available with aphid-transmitted viruses suggest that there 
can be a reduction in disease incidence, non-susceptible crops providing some separation and 
acting as a barrier against the infestation of a susceptible crop by incoming viruliferous vectors 
(Zitter & Simons, 1980; Thresh, 1952). 
In this paper, we present the results of a preliminary investigation on the effects of mixed 
cropping on the spread of ACMV. Among the virtually infinite number of crop permutations, 
cassava and maize were chosen for study as this is a very common association in Africa and 
elsewhere (Sylvestre & Arraudeau, 1983). 
h4ATERIAL AND METHODS 
The experiments were conducted in 1986 at the experimental farm of the Adiopodoumé 
ORSTOM research station, 20 k m  west. of Abidjan (Ivory Coast). The cassava variety used was 
"Aïpin Valenca" and has some resistance both to the disease and to the vector (Fargette, 1985). 
The CIMMYT maize variety used was "Amerillo sentendo" which has a 100 to 105 day growth 
period. Seven treatments were tested ; Cassava was planted either in monoculture (control plots) 
or interplanted with maize at two densities and on three dates (Table 1). The heights and the 
architecture of the crops differed widely between treatments according to the date and density of 
maize (Table 2). Crop canopies are known to be a critical factor influencing air movement and in 
consequence whitefly dispersal and virus spread (Fargette, Fauquet, Fishpool & N'Guettia, 
1988). Randomization of the treatments was therefore avoided as it would inevitably lead to 
interference between neighbouring plots of different treatments. A systematic arrangement was 
adopted with the seven elongate plots orientated along the direction of the prevailing south- 
westhorth-east wind which is the main factor influencing patterns of spread (Fargette, Fauquet 
R: Thouvenel, 1985). One plot was used for each treatment and was subdivided into 7 sub-plots 
of 9 x 9 m. For each treatment the cassava plants were inserted among the rows of maize which 
was planted at 28000 and 14000 plants per hectare corresponding to 25 and 50 cm spacing in 
rows. Planting dates were 18th of March, 28 March and 7th of April. Cassava was planted on 
the 28th of March at a density of 6000 plants per hectare, ie. 60 plants per plot at l m  spacing in 
rows 1.5 m apart (Table 1). The treatments were designated ]/E, IN, 1L, h/E, hh4, h/L, 1 and h 
for low and high maize density and E, M, L for Early, Medium and Late maize planting date, 
respectively. Monoculture is designated as M. 
Table 1. Details of the seven experimental treatments 
Maize density Low density High density 
Mid Late Mono Late Mid Early 
2813 7/4 2813 1 813 
h/E 
Planting date Early 
18/3 
Designation VE l/M VL M 
Disease incidence was based on weekly records of symptoms. Diseased plants were not 
removed. Whitefly populations were estimated weekly on 10 plants of each sub-plot of each 
treatment. Similarly, cassava growth was followed every two weeks by recording stem height 
and diameter. The heights of the maize plants were measured every two weeks'on 10 plants of 
each sub-plot of each treatment. 
RESULTS 
Maize and cassava growth. Table 2 indicates the mean height of the maize and the cassava plants 
for each treatment one, two and three months from planting. Not surprisingly, at each density 
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the earlier the maize planting, the higher the maize. The greatest differences in height were at one 
month as the most rapid growth occurs during the first month. Despite the large differences of 
maize height, maize was always taller than the cassava. 
Table 2. Heicht of the maize and of the cassava in the seven treatments one, two and three 
months after planting 
Treatment E 1/M 1/L M h/L h / M m  
1 month Maize 150 94 35 41 100 165 
Cassava 24 24 24 24 24 24 24 
2months Maize 227 217 177 182 222 242 
Cassava 196 106 101 91 106 121 106 
3 months Maize 227 225 222 222 232 242 
Cassava 172 192 187 167 192 202 182 
Temporal pattern of spread. Fig.1 illustrates the incidence of ACMV with time which differed 
between treatments.*Greatest spread occurred in mixed plantings with maize at low density sown 
early (E); it reached 67% four months after planting and the difference from the monoculture 
could be observed as early as two months after planting. 
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Fig. 1. Disease progress curve in each of the seven treatments 
Disease incidence was also consistently higher than monoculture in plots l/M and h/J3 although 
the difference was less (48% and 46% respectively vs 36% for the monoculture control, four 
months after planting). Disease incidence was similar to the control in trearment 1/L and h/M and 
lower in treatment h/L. 
Suatial distribution of the disease. Disease incidence four months after planting across the seven 
sub-plots of each treatment (ie. along the South-WestNorth-East axis) is illustrated in Fig.2a,b. 
Infection in the monoculture followed the typical pattern of distribution observed in previous 
studies (Fargette et al., 1985) with a decrease of disease incidence from the upwind margin into 
the middle of the field and a slighter increase at the downwind edge (Fig.2a). Higher disease 
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incidence in the upwind exposed plots was also observed in plots with maize at low density of 
planting, although it was more apparent in plots IlE and IL than in plot W. 
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Fig.2a.Disease incidence along: the SW/hE axis in dots with low maize density and in 
monoculture four months after ~lantinp 
Fig.2b.Disease incidence along the SW/NE axis in  lot^ 
with high maize density four months after plantinp 
By contrast, marked contrats in disease incidence were not observed in the n-eatments with high 
density of maize as the spatial dishibution of the disease was more or less random along the 
South-WestNorth-East axis (Fig.2b). 
Disease incidence and whiteflv ~ouulation. Fig.3 illustrates for the entire trial (all treatments 
combined) the weekiy average number of whitefly per plant and the percentage of plants first 
developing symptoms. Largest populations of whiteflies occurred in Iate April and in early May 
followed by a steady decrease. The curve of the weekly increment in diseased plants followed a 
similar trend with a delay of two weeks, the greatest increment occurring in mid-May indicating 
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that, taken. overall, it was the size of the whitefly population that was the main factor determining 
the rate of virus spread. 
Fig.4 illustrates the average number of whitefly recorded for each treatment. Different 
patterns of distributions were observed among the treatments. A peak of 30-40 whiteflies per 
plant was observed at low maize density in early May for each planting date (FigAa). 
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1614 3014 1415 2715 1016 2316 717 2117 
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Fig.3. Average weeklv number of whiteflies per Dlant (points) and weeklv percentace of plants 
showinE svmDtoms (histoflams1 
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Fig.4a. Averaee weekly number of whiteflies in do ts  
planted with a low maize density and in monwculhlr~ 
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By contrast, the number of whiteflies never exceeded 20 whiteflies per plant in either the control 
plat or high maize planting density plots (Fig.4b).The situation i n  plot h/E was atypical as low 
populations of whiteflies but high disease incidence were recorded. 
f P - - I  o ..,I \ 
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1614 3014 1415 2715 1016 2316 717 2117 
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Fig.4b. Average weeklv number of whiteflies in plots planted with a high maize density and in 
monocul ture 
Cassava aowth. Cassava growth was less than in the monoculture control in plots l/E, h/E, 1/M 
and l/M corresponding to the early or intermediate date of planting. This is likely to be due to the 
competition for light and available numents with the maize intercrop. No differences were 
observed between the control and the treatments with late maize, where competition may have 
been more limited. However no clear relationship between the pattern of growth and disease 
spread was observed among the treatments. 
DISCUSSION 
These results suggest that the spread of ACMV in mixed cropping systems can indeed be 
different from that in a cassava monoculture. Not only the temporal but also the spatial pattern of 
the disease as well as the dynamics of the vector were modified. The effects of mixed cropping 
on ACMV incidence seem complex. They cannot be due simply to protection of the cassava by 
the taller maize against the incoming viruliferous vectors as sometimes inferred for aphid-' 
transmitted viruses (Zitter & Simons, 1980; Thresh, 1982). The presence of maize did not 
always reduce the incidence of ACMV and higher incidences occurred in some maize/cassava 
combinations compared with the monoculture. Similarly, large accumulations of whiteflies and 
much spread of ACMV have occurred in a cassava field surrounded by a 3 m high sugarcane 
wind-break (Fargette et al., 1985). 
Our results suggest that the density rather than the height of the maize barrier affected the 
distribution and incidence of the disease and indicate that the differences of disease incidence are 
mainly due to changes in the sizes of whitefly populations. However, in a few plots the 
relationship between whitefly populations and disease incidence was atypical, suggesting that 
other factors -possibly the activity of the vector- can further modify the course of the epidemics 
in %xed cropping. Indeed, multiple cropping systems are known to affect insects dynamics at I 
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various stages including the colonisation of the crops, the developments of populations, the 
dispersal and the abundance of natural ennemies (Pemn, 1977). The overall effect on insect 
populations is complex and variable and it can result either in an increase or in a decrease in size 
of the population, depending on the pest species, the plants involved in the mixed cropping and 
the spatio/temporal combinations (Pemn, 1977). The two-week lag between vector populations 
and disease increment was shorter that in other field experiments (Fargette, 1985).,This may be 
because most spread occurred early in this experiment at a stage when plants are more vulnerable 
and soon develop symptoms. Modifications of growth induced by mixed cropping do not clearly 
affect the incidence of the spread, although it has been shown elsewere that susceptibility to . 
ACMV can be influenced by growth pattern (Fargette & Fauquet, unpublished results). 
At this stage of research we cannot clearly explain the factors goyeming spread in mixed 
cropping. Experiments carried out in monocultures have shown that the architecture'of the 
-cassava has profound effects on wind characteristics, vector movement and ACMV spread 
(Faqette et al., 1988). In addition, the height, orientation and permeability of a barrier is known 
to influence' wind profiles and insect distribu tion (Lewis and Stephenson, 1966). Additional 
information on the effects of maize barriers on wind characteristics, dynamics of population and 
vector movement is required before going further into these hypotheses in relation to ACMV and 
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" whiteflies. 
Our experiment should be considered as preliminary. Firstly, we are aware that the pattern of 
planting adopted is an oversimplication of intercropping in field situations. Usually more than 
two species are grown and the different species are not planted systematically as the densities, 
spacings and dates of plantings are highly variable. Therefore the hypotheses suggested above 
cannot be extended immediately to other multicropping systems. Secondly, it is difficult to adopt 
an appropriate experimental design for this type of study. The "cryptic error" due to interplot 
interference (Vanderplank, 1963) is known to be important with aerially-disseminated pathogens 
in general (Paysour & Fry, 1983) and in this type of experiment in particular. Wind breaks are 
known to affect wind speed over distances up to 10-20 times their height (Pedgley, 1982). To 
ensure independence between the experimental plots would imply an isolation of 20 to 40 metres 
between the plots. Such isolation is likely to increase environmental variability (Minogue, 1986) 
and would be difficult to provide in a limited area if several treatments, each with several 
replicates, are to be tested and. By separating the treatments, our design limited the 'cryptic 
error' but it had other limitations and precludes statistical analysis of the hypotheses suggested 
which should hence be considered as tentative. Further work in which special attention is given 
to various experimental designs should be carried out to validate these hypotheses. 
However, the results of this preliminary experiment reinforces the idea that epidemiology in 
multiple cropping is complex and should receive more attention, especially on methodology. The 
practical implication of the differences observed between spread in monoculture and mixed 
cropping suggests that caution is necessary in drawing conclusions from expenmental trials 
carried out in monoculture. Underestimation or overestimation of the spread to be expected in 
farmers fields could lead to incorrect advice being given on control strategies in general and on 
the level of field resistance to be used in particular. 
ACKNOWLEDGMENTS 
We thank Miss E. Servajean for field work, Dr. J.M. Thresh for constructive,criticism of the ., 
manuscript and Dr J.W. McNicol for helpful1 discussions. 
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A preliminary study on the influence of intercropping maize and cassava on the spread of African cassava mosaic virus by whiteflies

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