Why does the apple scab fungus still resist treatments?

Venturia inaequalis is the microorganism that causes apple scab, the familiar red blemish on fruit. Over the past two years, scientists surveyed 97 sites in Germany's Lower Elbe region to track how the fungus becomes resistant to chemicals. They examined 35 orchards under Integrated Pest Management (IPM), 16 with susceptible varieties, 12 with resistant (Vf) cultivars grown organically, and 34 abandoned sites.

No resistance was found to the newer SDHI fungicides (fluopyram, fluxapyroxad) despite more than five years of regular use. Resistance to anilinopyrimidines (cyprodinil, pyrimethanil) has also vanished after fifteen years. However, a few IPM orchards showed reduced sensitivity to dodine, and over 50% of susceptible trees displayed double resistance to two older groups: the MBC (thiophanate‑methyl) and the QoI (trifloxystrobin).

This double resistance persists decades after the chemicals were stopped, especially in the core ‘Altes Land’ area where intensive practices have fostered a uniform pathogen population. More isolated orchards host a more diverse fungus. The takeaway is clear: to keep treatments effective, growers must rotate chemicals, adopt cultural practices, and continuously monitor resistance.

Venturia inaequalis is a biotrophic ascomycete that primarily colonizes the leaf surface of apple trees. Its life cycle includes conidial production, which germinates under high humidity, and the formation of asci, sexual structures that promote genetic diversity. Fungicide resistance is usually mediated by point mutations in target genes: for succinate‑dehydrogenase inhibitors (SDHI) mutations affect the SdhB subunit, while for QoI (cytochrome bc1 inhibitors) alterations occur in the cytb gene, most notably the G143A substitution.

For MBC fungicides, resistance often stems from mutations in the β‑tubulin gene, preventing the fungicide from binding to microtubules. The observed double resistance (QoI + MBC) suggests cumulative selection, where populations have accumulated multiple mutations after prolonged treatment cycles. The persistence of these mutations for decades indicates a low fitness penalty: resistant strains are not disadvantaged in the absence of fungicides, likely because the mutations do not significantly impair essential cellular functions.

Epidemiologically, the uniform distribution of resistant strains in the Altes Land core area aligns with high spore flow among neighboring orchards, facilitated by shared pruning and irrigation practices. Peripheral orchards, with fragmented landscapes and lower tree density, limit spore dispersal, fostering genetically distinct populations.

Implications for integrated management include using fungicides with diverse modes of action, rotating products at intervals of at least three years, and integrating non‑chemical strategies such as removing infected leaves, applying biocontrol agents (e.g., Bacillus subtilis), and selecting genetically resistant cultivars (Vf). Moreover, molecular monitoring via real‑time PCR for key mutations (G143A, F129L, β‑tubulin) can provide timely data to adjust treatment recommendations, reducing resistance buildup and extending the efficacy of available products.