RESUMEN
In South Africa, potato (Solanum tuberosum) late blight epidemics from 1996 to 2007 were caused by Phytophthora infestans clonal lineage US-1 (McLeod et al. 2001; Pule et al. 2013). Similarly, surveys on tomatoes in the mid-1990s only identified the US-1 clonal lineage in South Africa (McLeod et al., 2001). On potatoes, populations from the Southern Cape and Western Cape regions consisted of persistent mefenoxam-resistant populations (McLeod et al. 2001; Pule et al. 2013). Limited mefenoxam (R-enantiomer of metalaxyl) screening in 2021 in the Western Cape showed that potato isolates were sensitive, which prompted our study. Potato late blight samples were collected in 13 potato fields in the 2021 to 2023 seasons in the Western Cape (n = 4), Free State (n = 7), Limpopo (n = 1) and Kwazulu-Natal (n = 1) Provinces, and one tomato sample in 2022 in the Limpopo Province. Fourteen samples, one per field, were simple sequence repeat (SSR) genotyped for 12 loci (Li et al. 2013) using as DNA template, FTA cards, or genomic DNA extracted from cultures. P. infestans isolations from lesions and DNA culture extractions were conducted as previously described (Pule et al. 2013). SSR genotyping revealed that all 14 P. infestans samples belonged to clonal lineage EU_23_A1 (EU23), which has a phenotype (A1 and metalaxyl sensitive) and SSR genotype matching the US-23 lineage (Saville et al., 2021). As expected, minor polymorphisms were detected among the samples at loci Pi02, G11, D13 and SSR4. Mefenoxam sensitivity testing of seven potato isolates from the Free State (n = 3) and Western Cape (n = 4), and one tomato isolate was conducted as previously described (Mcleod et al. 2001). All isolates were sensitive to mefenoxam since no infection and sporulation occurred at 3 µg/ml. This was expected since EU23 has been reported as mefenoxam sensitive in other countries (Kawchuk et al., 2011; McGrath et al., 2015). Replacement of the US-1 clonal lineage by EU23 suggests that the latter lineage is more aggressive or fit than US-1, but this must be verified especially on potatoes. On tomatoes, on the other hand, EU23 is known as a highly aggressive lineage (Kawchuk et al., 2011; McGrath et al., 2015; Saville et al., 2021). Therefore, population displacements may have first occurred on tomatoes from where the lineage spread to potatoes. In the Cape coastal potato production regions, population displacement may have been supported by the withdrawal of mefenoxam/metalaxyl from the region since 1996 because the EU23 lineage is mefenoxam sensitive, as opposed to the previously prevailing US-1 mefenoxam-resistant lineage. More severe potato late blight epidemics has not been observed in recent years in South Africa. However, tomato late blight has increased and is more prevalent in the Limpopo province. The source of the introduction of EU23 into South Africa is unknown. Only test-tube plants and/or greenhouse tubers may be imported into South Africa since 1997. Therefore, the illegal importation of planting material may have introduced the new genotype. Whether this could have occurred from neighbouring African countries is unknown since P. infestans genotyping has not been conducted in these countries. In Africa, EU23 has been reported in northern African countries (Tunisia, Algeria and Egypt) (Saville et al., 2021; El-Ganainy et al., 2023). Mefenoxam and metalaxyl applications will likely be effective again in the Western Cape, but more samples will have to be tested to confirm this. This will provide growers with a more cost-effective fungicide (metalaxyl) since alternative actives with comparable systemic and curative activity are more expensive.
RESUMEN
Infection of grapes by different densities of airborne conidia of Botrytis cinerea was investigated on table grapes (cultivar Dauphine) harvested ripe (16°Brix) and inoculated fresh, or after SO2 treatment and 8-week storage at -0.5°C. Berries were detached at each inoculation and dusted with dry conidia in a settling tower. Following inoculation, the fresh berries were incubated for 24 h at high relative humidity (≥93%), or were overlaid with wet sterile paper towels. Cold-stored berries were incubated at high relative humidity. The effect of conidial density on surface colonization, penetration, and lesion formation was determined by surface sterilization, isolation, and freezing studies on fresh berries. Only symptom expression was determined on cold-stored berries. Fluorescence microscopy of skin segments showed that conidia were consistently deposited as single cells, and not in pairs or groups, on berry surfaces. Individual conidia, at all densities tested, readily infected the cold-stored berries and formed separate lesions after 2 days. Although the cold-stored berries were highly susceptible, lesion numbers were not related to conidial density at low inoculum dosages (0.67 to 2.60 conidia per mm2 berry surface). Lesion numbers tended to increase exponentially at higher dosages (3.24 to 3.88 conidia per mm2 berry surface). Individual conidia, however, did not induce any disease symptoms on fresh berries. Removal of the pathogen after 24-h incubation from the surface of fresh berries by ethanol, and subsequent incubation of excised skin segments revealed that, irrespective of the conidial density or the wetness regime, less than 2% of skin segments were penetrated. Furthermore, increasing densities of conidia did not lead to higher rates of surface colonization and skin penetration. The low incidence of disease caused on fresh berries and high disease incidence induced after prolonged cold storage indicated that infection was not governed by conidial density on berry surfaces, but by the level of host resistance.
RESUMEN
The occurrence of Botrytis cinerea and subsequent disease expression at different positions on leaves and bunches of grape was determined from 1996 to 2000. Different techniques were used to detect viable inoculum on material obtained from table (cvs. Barlinka and Dauphine) and wine grape (cv. Merlot) vineyards. Isolations were made from berry skins on Kerssies' B. cinerea selective medium or on water agar medium supplemented with paraquat. Leaves and parts of bunches bearing three to seven berries on a short rachis section were used untreated or treated with paraquat, or were frozen for 1 h at -12°C. Paraquat and freezing were used to terminate host resistance and to promote the development of the pathogen from the tissues. The material was used untreated to detect the pathogen on the surface, or were surface-sterilized to detect mycelia (latent infection) in the tissue. B. cinerea occurred in a consistent pattern in leaves and bunches in all vineyards. Based on the combined data for tissues exposed and unexposed to paraquat, B. cinerea occurred predominantly in bunches and was mostly associated with the bases of the berry and the pedicel. Overall, approximately 30% of the berries yielded B. cinerea at these positions. The next prominent positions occupied were leaf blades, rachises, and laterals, of which approximately 20% yielded B. cinerea. The pathogen occupied the petioles less often (10%), and the berry cheek infrequently (5%). The stylar end of the berries, on the other hand, was virtually free (0.02%) of the pathogen. Disease expression in bunches displayed the pattern showed by the inoculum ecology, and symptoms consistently developed first at the berry-pedicel attachment zone. The isolation studies showed that the pathogen seldom occurred on the surface or in the skin tissue near the base, cheek, or stylar end of berries. Latent infections in the berry base were also few at véraison and harvest. Collectively, the findings indicate that conidia dispersed in early season in bunches, and residing superficially at the berry-pedicel attachment zone, are a major factor in B. cinerea bunch rot.