Chemical control of botrytis and its resistance to chemical fungicides

Abstract

The chemical control of Botrytis spp., and especially B. cinerea the causal agent of grey mould on many crops, can be achieved by several families of fungicides. Among those affecting fungal respiration, the oldest ones are multi-site toxicants (e.g. dichlofluanid, thiram); newer ones are uncouplers (e.g. fluazinam), inhibitors of mitochondrial complex II (e.g. boscalid) or complex III (e.g. strobilurins). Within anti-microtubule botryticides, negative-cross resistance can occur between benzimidazoles (e.g. carbendazim) and phenylcarbamates (e.g. diethofencarb), a phenomenon determined by a mutation in the gene encoding -tubulin. Aromatic hydrocarbon fungicides (e.g. dicloran), dicarboximides (e.g. iprodione, procymidone, vinclozolin) and phenylpyrroles (e.g. fludioxonil) affect the fungal content of polyols and resistance to these various compounds can be associated with mutations in a protein histidine kinase, probably involved in osmoregulation. However, dicarboximide-resistant field strains of B. cinerea are sensitive to phenylpyrroles. Anilinopyrimidines (e.g. cyprodinil, mepanipyrim, pyrimethanil) inhibit methionine biosynthesis but their primary target site remains unknown. In few situations, resistance of commercial significance has been recorded. Among sterol biosynthesis inhibitors those inhibiting 14- demethylase (DMIs) which are widely used against many fungal diseases are of limited interest against Botrytis spp., whereas the hydroxyanilide fenhexamid, which inhibits the 3-keto reductase involved in sterol C4-demethylations, is a powerful botryticide. Monitoring conducted in French vineyards revealed the presence of multi-drug resistant (MDR) strains, a phenomenon probably determined by overproduction of ATP-binding cassette transporters. Resistance towards fungicides of the different groups is described throughout the chapter. © 2007 Springer Science+Business Media B.V.