ABSTRACT
Banana bunchy top disease (BBTD), caused by the banana bunchy top virus (BBTV, genus Babuvirus), is the most destructive viral disease of banana and plantain (Musa spp.). The virus is transmitted persistently by the banana aphid, Pentalonia nigronervosa Coquerel (Hemiptera: Aphididae). While research efforts have focused on screening Musa genotypes for BBTD resistance, comparatively little work has been carried out to identify resistance to banana aphids. This study assessed 44 Musa germplasm of different A and B genome composition for the performance of banana aphids under semicontrolled environmental screenhouse conditions and in a field trial established in a BBTD endemic location. In the screenhouse, the AA diploid Calcutta 4 had the lowest apterous aphid density per plant (9.7 ± 4.6) compared with AAB triploid Waema, which had the highest aphid densities (395.6 ± 20.8). In the field, the highest apterous aphid density per plant (29.2 ± 6.7) occurred on the AAB triploid Batard and the lowest (0.4 ± 0.2) on the AA diploid Pisang Tongat. The AA diploid Tapo was highly susceptible to BBTD (100% infection) compared with the genotypes Balonkawe (ABB), PITA 21 (AAB), Calcutta 4 (AA), and Balbisiana Los Banos (BB), which remained uninfected. The Musa genotypes with apparent resistance to BBTD and least susceptibility to aphid population growth provide options for considering aphid and BBTD resistance in banana and plantain breeding programs.
ABSTRACT
BACKGROUND: Evolution of pyrethroid resistance in the cotton bollworm Helicoverpa armigera (Hübner) (Lepidoptera: Noctuidae) threatens continued cotton production in Central Africa. Dose-response bioassays were conducted on area-wide collection of bollworm populations from major host plants, while biochemical techniques were used to evaluate basic mechanisms underlying resistance. RESULTS: Pyrethroid resistance is primarily associated with detoxification by enhanced esterase activity. High resistance to cypermethrin (RF = 67-1771), cross-resistance to deltamethrin (RF = 60-2972) and lack of cross-resistance to the non-ester pyrethroid etofenprox (RF = 2-10) were observed among H. armigera field populations and laboratory-selected strains. Enzymatic assays showed that esterase activity, but not oxidase content or glutathione-S-transferase activity, was positively correlated with resistance to cypermethrin. Pretreatment with piperonyl butoxide (PBO) resulted in significant synergism with cypermethrin in 6/10 field populations, but not in the laboratory-selected strain, indicating that additional mechanisms such as mixed-function oxidase (MFO) may be involved in field resistance. The absence of cross-resistance to DDT ruled out a possible target-site modification. CONCLUSION: Knowledge of the mechanisms involved in pyrethroid resistance and the lack of cross-resistance to spinosad and indoxacarb is a key to devising new resistance management strategies aimed at restoring the efficacy of pyrethroid-based programmes.