368 J.L. BECKERMAN AND G.W. SUNDIN
the era of synthetic fungicides and would soon change management
practices, and ushered in the beginning of the era of synthetic fungi-
cides. Within the decade, advances in sprayer technology improved
applications so that more of the fungicide remained on the leaf, instead
of running off, along with new classes of fungicides that prevented
tissue invasion by the scab fungus after infection had occurred. New
fungicides, such as mancozeb and captan, further improved scab man-
agement. These fungicides better protected tissue from invasion by the
scab fungus, and could also stop infection during a limited time after it
had occurred, as indicated by Mills infection table (Sutton 1996; Cooley
2009).
These successes further improved with the introduction of fungi-
cides that could arrest fungal growth for 48 h or more after infection
had occurred. The first of these fungicides included dichlone, lime
sulfur, and mercury; more recently introduced fungicides with after-
infection activity include dodine and the methyl benzimidazole car-
bamates (MBC), sterol biosynthesis or demethylation inhibitors (SBI),
anilinopyrimidines (AP), and strobilurin or quinone-outside inhibitors
(QoI). Growers could apply these fungicides in response to the likeli-
hood of infection, as opposed to the possibility of it because of poten-
tially favorable weather conditions. More importantly, fungicides could
be applied after a rain event, but still within a window that allowed
eradication. Prior to the development of these fungicides, growers were
advised to protect trees prior to rain events, despite the knowledge that
severe rain events (1–2 inches of rain, or rain events extending several
days) would reduce efficacy by 50–100%.
C. Evolution of Fungicide Resistance inVenturia inaequalis
The introduction of the systemic fungicide dodine (and later benomyl)
profoundly changed apple scab management, but a harbinger of future
problems arose until with the first reports of fungal resistance to these
fungicides in the late 1960s and early 1970s (Jones 1981). Fungicide
resistance is a phenotype that may result from single or multiple gene
mutations. Single-gene mutations, that confer resistance to site-specific
fungicides (like the benzimidazole fungicide, benomyl), are more likely
to develop than the simultaneous multiple gene mutations that are
needed to confer resistance to multi-site inhibiting fungicides (like cap-
tan or mancozeb). The selection of fungicide resistance is an evolution-
ary process that results when those isolates that possess a genetic muta-
tion that provides the efflux, transport, or detoxification of the fungicide
survive and reproduce, despite the presence of fungicide (the selective