African Crop Science Journal African Crop Science Society ISSN: 1021-9730 EISSN: 2072-6589 Vol. 8, Num. 2, 2000, pp. 179-186

African Crop Science Journal, Vol. 8. No. 2, pp. 179-186

FIELD REACTION OF CASSAVA GENOTYPES TO ANTHRACNOSE, BACTERIAL BLIGHT, CASSAVA MOSAIC DISEASE AND THEIR EFFECTS ON YIELD

C.N. Fokunang, T. Ikotun, A.G.O. Dixon¹ and C.N. Akem¹
Department of Crop Protection and Environmental Biology, University of Ibadan, Oyo State, Nigeria
¹International Institute of Tropical Agriculture, PMB 5320, Oyo Road, Ibadan, Nigeria

(Received 9 October, 1998; accepted 20 January, 2000)

Code Number: CS00019

INTRODUCTION

Cassava, Manihot esculenta Crantz, is one of the least risky food crops in Africa because of its ability to tolerate and recover from drought, disease and pest attacks when favourable conditions return (Hahn and Keyser, 1985). Yields are reasonable even under marginal soil conditions, and both storage roots and leaves are available all the year round (IITA, 1990). Research in cassava production show that the crop is susceptible to at least thirty different fungal, bacterial, viral and mycoplasma diseases (Theberge, 1985; IITA, 1990). Of these diseases, cassava mosaic (CMD), bacterial blight (CBB) and anthracnose (CAD) are of major economic importance.

Cassava mosaic disease (CMD). The etiology of CMD is well established, being incited by geminiviruses of which at least three have been distingusihed (Thresh et al., 1994; Harrison et al., 1997). CMD is readily transmitted by a whitefly Bemisia tabaci Genn, and disseminated in cuttings from infected plants (Fauquet and Fargette, 1990; Thresh et al., 1997). Transmission of CMD to cassava plants depends upon the availability of inoculum and the population density and activity of the whitefly. CMD causes storage yield reductions of 20-60 percent, and in some cases total crop failure (IITA, 1990; Otim-Nape et al., 1994).

Cassava bacterial blight (CBB). This disease is host specific and restricted to cassava (Ikotun, 1981). The causal agent, Xanthomonas campestris pv. manihotis (Berthet and Bondar), has been reported in many countries throughout Africa. CBB can cause complete yield loss under conditions favourable for the development and spread of the causal pathogen (Lozano, 1986; Boher et al., 1995). The major means of spread of the disease is by movement of infected planting materials, and rapid field infection is caused by rain-splash (Elango and Lozano, 1981; Verdire et al., 1997).

In areas of Africa where there are distinct rainy and dry seasons, the disease cycle of CBB consist of two phases, an angular leaf spot phase and an epiphytic phase. The angular leaf spot phase begins soon after the first rains and continues during the rainy season. This is followed by wilting and defoliation of infected leaves, tip die-back and death of the plant in susceptible varieties (Lazano, 1986). The epiphytic phase begins with onset of the dry season when the pathogen has survived the dry season of 5-6 months as an epiphyte and increase in number with the availability of moisture (Hahn et al., 1989; Boher et al., 1995).

Cassava anthracnose disease (CAD). This disease, incited by Colletotrichum gloeosporioides f.sp. manihotis, is an epidemic disease characterised by particular symptoms (cankers on stems, branches and fruits, leaf spots and tip die-back) on aerial parts of the diseased plants (Makambila, 1987). The appearance of the disease depends on the cassava variety and the infected plant parts.

In older stems, CAD infection usually occurs as round and stringy lesions, which develop into deep cankers. Stem deformation occurs in some cultivars, making the stems brittle and easily broken by wind action (Ikotun and Hahn, 1992). Deeper cankers sometimes affect the pith of the plant, resulting in blocked circulation (van der Bruggen and Maraite, 1987). CAD can cause significant loss in planting materials and total crop failure (Makambila, 1987). Severely infected stems and seeds in some cases result in a decrease of 20-45% germination (IITA, 1990; Fokunang et al., 1999).

Given the importance of these diseases and on-going effort to develop effective management systems, this study was conducted to assess the reaction under field conditions of some cassava genotypes to CMD, CBB and CAD and the effects of the diseases on crop yield.

MATERIALS AND METHODS

Experimental site. The study was conducted at the International Institute of Tropical Agriculture (IITA), Ibadan, Nigeria. The planting materials were collected from the cassava germplasm selection of the Tuber and Root Crops Improvement Programme (TRIP) of IITA.

Field evaluation of incidence and severity of CAD, CBB and CMD. Thirteen cassava genotypes were used for this study. The disease incidence and severity of CAD, CBB and CMD were evaluated 3 and 6 months after planting, in three consecutive planting seasons. Plantings were made in May of 1992, 1993 and 1994. Planting was done in rows of ten plants per clone in four replications, arranged in a randomised complete block design. Disease severity scores were based on observations of disease symptoms on naturally infected plants as follows:

Cassava anthracnose disease (CAD). This was scored on a scale of 1-5 as adopted from Muimba (1982), where: 1= no symptoms; 2= development of shallow cankers on stems, on the lower part of the plants; 3= development of successive cankers higher up the plant, with cankers on older stems becoming larger and deeper; 4= development of dark-brown lesions on green shoots, petioles and leaves, collapse and distortion of young shoot; and 5= wilting, drying up of shoots and young leaves, death of part or whole plant.

Cassava bacterial blight (CBB). This disease was scored on a scale of 1-5 (Muyolo, 1984), where; 1= no symptoms; 2= only angular leaf spots; 3= extensive leaf blight and leaf wilt, defoliation, gum exudate on stem and petioles;

4= extensive leaf blight, wilt defoliation and stem die-back; and 5= complete defoliation and stem tip die-back of lateral shoot.

Cassava mosaic disease (CMD). Disease severity on plants was assessed by rating the symptom expressed on six topmost leaves of one shoot per plant. The rating method was based on a score of 1-5 (Hahn et al., 1980) where: 1= no symptoms observed; 2= mild chlorotic pattern over entire leaflets or mild distortion only at base of leaflets with the rest of the leaflets appearing green and healthy; 3= conspicuous mosaic pattern throughout leaf, narrowing and distortion of lower one-third of leaflets; 4= severe mosaic, distortion of two thirds of leaflets and general reduction of leaf size; and 5= severe mosaic, distortion of four-fifth or more leaflets, twisted and misshapen leaves.

Disease incidence for CAD, CBB and ACMD in any particular test was calculated as percentage of diseased plants in each test genotype trial in the field.

Yield assessment. All the cassava genotypes were harvested 12 months after planting and assessed for yield by recording storage root number, storage root weight, dry matter content and tuber rots. The storage root number in each row of the cassava genotype was counted and recorded, while the storage root weight (yield) was taken by weighing each plot row of cassava genotype harvested. Tuber root rot was recorded as the number of rotted tubers in each harvested plot row per genotype. Dry matter content of storage roots, was recorded from 200 g of fresh crushed materials of each cassava genotype dried at 60°C to constant weight.

Statistical analysis. Data were subjected to analysis of variance (SAS Institute, 1989). Where the anova test indicated significant differences, treatment means were separated using Fischer’ protected least significant difference (LSD) at 5% probability level. Correlation analysis was done to establish the relationship among the diseases and between disease severity and yield.

RESULTS

Yield of cassava genotypes over 3 planting seasons (1992, 1993, 1994). The pooled means of yield parameters over the 3 years showed significant differences (P<0.05) in plant stand, storage root number, fresh root weight and percentage tuber dry matter among the cassava genotypes (Table 1). The highest storage root number of 61.6 plot-1 was recorded for genotype 88/01087, while the lowest mean number of 19.4 per plot was recorded for genotype 91/00016. The highest mean storage root weight of 19.4 kg plot-1 was recorded for genotype 88/01983, with the lowest mean storage root weight of 3.9 kg plot-1 recorded for genotype 91/00016. Mean percentage tuber dry matter was least in genotype 90/00333 (18.9%), while a mean maximum of 30.7% was recorded for genotype 91/00396 (Table 1). Tuber root rot showed no significant variation among the cassava genotypes at twelve months after planting. More than 80% of the tested genotypes showed no incidence of root rot.

Disease reactions. Field evaluation was made on the reaction of cassava genotypes to CAD, CBB and CMD in three consecutive planting seasons.There were significant differences between genotypes in CAD, CBB and CMD symptom expression in the three plantings. Overall, mean CAD incidence was highest (59.4%) in 1993 and lowest (25.1%) in 1994 (Table 2). CBB incidence was generally low in all three plantings, with the highest overall mean incidence of 39.7% recorded in the 1994 planting. Highest mean incidence of CMD (71.2%) was recorded in 1992, while the lowest mean incidence of 60.5% was recorded in the 1993 planting.

CAD, CBB and CMD severity differed significantly (P<0.05) among the genotypes in each of the three plantings (Table 3). Highest overall mean CAD severity score of 2.6 was recorded in 1992 and the least score of 1.7 in 1994. The highest overall CBB mean score of 2.0 was recorded in 1992 and the lowest mean score of 1.7 in 1994. Highest overall mean CMD severity score of 2.7 was recorded in 1994, while the lowest overall mean score of 2.3 was recorded in 1993.

There was a significant positive correlation between CBB incidence and severity (r=0.66) (Table 4). CBB incidence and CMD incidences were not significantly correlated (r=0.03), whereas CAD and CMD incidences and severities were positively and highly significantly correlated (r=0.82 and r=0.76, respectively). CAD and CBB incidence and severity were also significantly correlated (r=0.47 and r=0.43, respectively).

Correlation analysis between yield parameters and disease symptom expression showed a significant negative correlation between CBB incidence and storage root weight (r=-0.45), and storage root number (r=-0.48) (Table 5). Correlation of CAD severity on storage root yield and percentage DM was not significant (r=0.21 and r=0.20, respectively). CBB severity was not significantly correlated with percentage DM (r=0.22), but negatively correlated with storage root number (r=-0.44) and yield (r=-0.43). CMD severity also showed a significant negative correlation with yield (r=-0.44).CAD severity had no significant correlation with yield (r=0.21) and percentage DM (r=0.20).

DISCUSSION

Field evaluation of cassava genotypes showed significant variation in disease incidence and severity for CAD, CBB and CMD amongst the genotypes, across the three planting seasons. This evaluation could support the multiple resistance screening of the genotypes to these diseases under natural conditions. The highly significant correlation observed in CBB and CAD incidence and severity among the genotypes suggest possible synergistic relationship of the two pathogens.

Muyolo (1984) reported synergistic relationship between CBB and CAD pathogens among cassava clones inoculated in nurseries and screenhouse trials. This relationship in severe infection conditions could lead to a disease complex, which creates difficulty in distinguishing the two diseases in the field. Hahn et al. (1980) reported that transmission of CMD from one cassava plant to another depends on availability of inoculum and the population density and activity of whitefly (Bemissia tabaci) vectors. Favourable environmental conditions (high relative humidity and abundant rainfall) in the wet season, when cassava cultivation is intense and crop growth luxurious, favours whitefly population build-up (Theberge, 1985) and increased CAD vector activities (Boher et al., 1983), and creates a favourable medium for X. campestris pv. manihotis infection in the field (Lozano, 1986).

Severity of cultivar infection also depends on the susceptibility or resistance of host plants. Severely infected cassava cultivars show stunted growth, poor biomass production and low yield. They also yield less planting materials for the next season (IITA, 1987).

The significant positive correlation between CMD and CBB in this study supports earlier reports by Hahn et al. (1989) of a significant genotypic correlation between resistance to the two diseases (r=0.90), and suggested that the relationship could be due to linkage. Msabaha (1981) also reported that the genotypic correlation between CMD and CBB vary from 0.7 to 1.4 on cassava seedlings and from 0.5 to 0.7 on plants raised from cuttings. Due to this genotypic correlation between CMD and CBB, selection for resistance to either of the disease in a breeding programme could result in a genetic progress in resistance to the other disease. Cassava genotypes TMS 30001, 30211 and 88/01087 showed a stable resistance over the 3 planting seasons to CAD, CBB and CMD.

The correlation between growth parameters, disease incidence and severity showed that there was a significant negative correlation between CBB and yield (r=-0.42) and root tuber number (r=-0.43). CAD severity on yield and dry matter was not significantly correlated. In this study, variability in disease incidence and severity and the influence on yield is also linked to genotype-environmental interactions, which have a combined influence on epidemiology of the diseases in the field.

ACKNOWLEDGEMENTS

The authors are grateful to the Training Programme, International Institute of Tropical Agriculture (IITA), Ibadan, Nigeria for the financial assistance for this work, and the Tuber and Root Crops Improvement Programme (IITA) for their technical assistance. The anonymous reviewers of the manuscript are also gladly acknowledged.

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