Unfortunately, there are few general rules for managing fungicide resistance. First, the fungicides themselves vary widely in their biochemical modes of action and the spectrum of organisms against which they are effective. Secondly, different fungi differ widely in their capacity to produce fungicide resistant biotypes. If we truly want to manage resistance, we must consider each fungus and each fungicide on a case-by-case basis.

There are several factors that affect the rate at which the frequency of fungicide resistance increases to the point where disease control becomes a problem. The first is the initial frequency of resistant individuals in the fungal population. It matters little whether those individuals existed before the fungicide was used or whether a fungicide-resistant biotype arose by a chance mutation some time after the fungicide had been in use. In either case, what is important is the proportion of the propagules of the fungus that are of the resistant (or, if you prefer, "less sensitive") biotype at any point in the epidemic.

The second factor is the rate of selection of the resistant biotype, that is, its relative success in surviving and reproducing (compared with the sensitive biotype) in the presence of the fungicide. This is affected by the dose of the fungicide (the higher the dose, the less chance for "escapes" of the sensitive biotype) and by the level of resistance expressed in the resistant biotype. For example, if the lethal dose for the resistant biotype were 100 times that required for the "wild type", we would expect to see a faster rate of selection than if the resistant biotype were killed by only twice the dose required to kill the wild type.

The third factor is the fitness of the resistant biotype relative to the sensitive biotype in the absence of the fungicide. This affects the rate at which the resistant population "reverts" to the wild type without continued selection by the fungicide to which it is resistant. The effect of fungicide resistance on the fitness of the fungus varies quite widely, depending on the biochemical basis of resistance. For example, many fungi resistant to benomyl seem to be nearly as ecologically fit as their benomyl-sensitive counterparts, whereas some of the fungi resistant to some of the dicarboximide fungicides appear to gain that resistance only at great metabolic cost, and they are far less able to compete in the absence of the fungicide than are their corresponding wild types.