Item Details

Title: Influence of Host Plant Resistance and Disease Pressure on Spread of Cassava Brown Streak Disease in Uganda

Date Published: 2015
Author/s: K. Katono, T. Alicai, Y. Baguma, R. Edema, A. Bua and C. A. Omongo
Data publication:
Funding Agency : MSI- Uganda (Grant No. MSI / WAI / 02/08)
Copyright/patents/trade marks:
Journal Publisher: American Journal of Experimental Agriculture
Affiliation: College of Agricultural and Environmental Sciences, Department of Crop Production,
Makerere University, P.O.Box 7062, Kampala, Uganda. 2
National Crops Resources Research Institute (NaCRRI), Namulonge, Root Crops Programme,
P.O.Box 7084, Kampala, Uganda
Keywords: CBSD; disease pressure zones; whitefly; Bemisia tabaci; Uganda

Abstract:

Cassava brown streak disease (CBSD) is a major constraint to cassava production in Uganda. The
disease is caused by two ipomovirus species: Cassava brown streak virus (CBSV) and Ugandan
cassava brown streak virus (UCBSV), both transmitted by the whitefly vector (Bemisia tabaci).
Since the outbreak of the CBSD epidemic in Uganda in 2004, knowledge of its spread in the field is
still limited. In this study, five cassava genotypes with varying levels of resistance to CBSD: TME
204 (susceptible), I92/0067, MH 97/2961, MH 96/0686 (moderately tolerant) and NASE 3 (tolerant)
were used to evaluate the effect of genotype and prevailing disease pressure on CBSD spread in
Uganda. The experiment was established in a randomized Complete Block Design (RCBD) in three
sites of varying CBSD disease pressure: high (Wakiso), moderate (Kamuli) and low (Lira) in November, 2009 to November, 2010. Disease incidences (%), apparent infection rate (r), area
under disease progress curves (AUDPC) were determined and population of the whitefly vector
monitored monthly for 8 months. Genotype and disease pressure significantly affected CBSD
incidence (P = .001), with Lira recording no noticeable disease spread even in the susceptible
genotype TME 204. On the contrary, in Wakiso and Kamuli final disease incidence was maximum
(100%) in the genotypes I92/0067, TME 204 and MH 97/2961 while the tolerant genotype NASE 3
had low final disease incidence of = 5%. Mean whitefly population varied with site (P = .001) and
there was a positive interaction between whitefly population and disease pressure hence the rapid
CBSD spread in Kamuli and Wakiso. There was a high correlation (r = .994) between foliar and
root CBSD incidence hence high CBSD root incidence in Kamuli and Wakiso. From these results, it
is evident that high disease pressure, use of susceptible genotypes and high whitefly population
significantly enhanced CBSD spread and development.