| Popis: |
The way in which fungal populations respond to fungicides used for their control, and hence the risk of disease control failures due to resistance, depends primarily on the type of genetic variability available. Existing evidence indicates that the type of variability differs with the chemical rather than with the organism. With most systemic fungicides and antifungal antibiotics, high resistance can be obtained by mutation of a major gene. The population response is then qualitative and a high or moderate resistance risk is involved, depending on the effect of the major gene on fitness. Mathematical models are available, on the basis of which the establishment of resistance and the loss of effectiveness of a fungicide of this group can be predicted. With a few systemics and some protectants, a practically significant decrease of sensitivity requires the interaction of several genes, each of a rather minor effect: the response is quantitative and the resistance risk is low th moderate. In this situation, the combination of degree of resistance and fitness loss varies greatly and this has not permitted the construction of suitable mathematical models so far. Finally, there is no evidence that pathogenic fungi possess genes for resistance to most protectant fungicides, which involve a low resistance risk, if any. Selection of forms less sensitive to fungicides of this group does not seem to have taken place, in spite of many years of repeated use. |
