Resistance to fungicides is a normal phenomenon embodied in the natural process of the evolution of biological systems. By close co-operation of the agrochemical industry and researchers, advisers and growers we can ensure that fungicides are used optimally and continue to offer the benefits they currently confer.
Resistance to SBI fungicides has been well characterized during the last 20 years. Issues with SBI performance typically became obvious only after numerous years of intensive use with efficacy degrading stepwise. Following reduced selection pressure, a partial recovery in sensitivity is often observed. The primary mechanism of resistance is the accumulation of several independent mutations in the target site. Each individual mutation typically causes only a small reduction in sensitivity and it is not until multiple mutations accumulate in an isolate that a large enough reduction in sensitivity is observed to impact efficacy under field conditions. Resistance to DMIs or Amines is mostly characterized by a slow, step-wise erosion of efficacy over several years of intensive use rather than by a rapid loss of control.
This type of step-wise resistance is called "multigenic", continuous”, “quantitative” or “shifting” type resistance (Fig. 1).
Fig. 1. General scheme of shifting-type resistance.
In addition to mutations at the target site, reductions in sensitivity of individual isolates can be also be attributed to overexpression of the cyp51 gene and transport away from the target site by ABC transporters. It is not clear how important these mechanisms of resistance are under field conditions as they often co-exist with mutations at the target site.
Resistance risk is generally considered to be
low to medium (amines, KRIs) or
Resistance development is typically correlated with a fitness penalty for less sensitive isolates. Partial back-shift is possible if selection pressure decreases.