Fusarium avenaceum: A Toxigenic Pathogen Causing Ear Rot on Maize in Yunnan Province, China

Ear rot of maize, caused by Fusarium spp., is one of the most destructive diseases, occurring in most maize-producing countries worldwide. In September 2016, typical symptoms of Fusarium ear rot were observed on maize with approximately 5 to 10% incidence in Qujing city, Yunnan province, China. Symptoms on the infected ears were white to pink or salmon-colored mold at the tip of the ear. Symptomatic kernels were sterilized and incubated on potato dextrose agar (PDA) plates supplemented with streptomycin sulfate (150 µg/ml) and kanamycin (150 µg/ml) for 4 days at 25°C. The fungal colonies displaying morphological characteristics of Fusarium spp. were subcultured on PDA and synthetic low-nutrient agar (SNA) plates as described by Shan et al. (2017). On PDA plates, aerial mycelia were compact and wooly, having white to light yellow color with central spore mass pale orange to brown, and the colony reverse was carmine. On SNA plates, macroconidia were usually produced on sporodochia. The macroconidia were thin walled, long, straight to slightly curved, extended bent apical cells with indented basal cells, and generally had 3 to 5 septa, usually on average 49.7 ± 9.2 µm long × 4.6 ± 1.0 µm wide. Microconidia were fusoid, 1 to 2 septate, and ranged from 13.4 to 24.6 µm long × 2.6 to 4.8 µm wide, similar to the description by Leslie and Summerell (2006). No chlamydospores were observed during the growing period. Species identification was further confirmed from two isolates, YNSF16-66 and YNSF16-68, by amplification and sequencing of partial sequences of the translation elongation factor gene (TEF1-α, EF1 and EF2 primers), the second largest subunit of the RNA polymerase gene (RBP2, 5f2 and 7cr primers), and partial sequences of β-tubulin (TUB2, βTUB-F1 and T22 primers) (Harrow et al. 2010; O’Donnell et al. 2010). BLAST analysis revealed that the partial sequences of the TEF1-α, RBP2, and TUB2 of the two isolates were 99% identical to those of F. avenaceum (GenBank accession nos. AB674293, GQ915486, and GQ915436, respectively). The new sequences of partial TEF1-α, RBP2, and TUB2 have been deposited in GenBank (accession nos. MK185024 to MK185029). Koch’s postulates were performed to determine pathogenicity using freshly harvested corncobs. For each isolate, the ears were wounded by a 1-ml sterile syringe needle and inoculated with 20 µl of conidial suspension of 10⁶ conidia/ml concentration as described by Kim and Woloshuk (2011). The inoculated kernels were maintained in a clear container within the greenhouse at 25 ± 0.5°C with high humidity. After 5 days, kernels inoculated with F. avenaceum exhibited discoloration and extensive mycelial growth with dark rose pigments on the surface, similar to those observed in the field. No symptoms were observed on any of the control kernels. The pathogen was reisolated from the symptomatic kernels but not from the control. In China, F. avenaceum has also been reported to cause root rot of maca (Lepidium meyenii) (Wei et al. 2017), bulb rot of Allium giganteum (Zhang et al. 2016), and fruit rot of Rubus idaeus (Wang et al. 2017). To the best of our knowledge, this is the first report of maize ear rot caused by F. avenaceum in China. Considering F. avenaceum can produce an array of mycotoxins including moniliformin, acuminatopyrone, and chrysogine (Sørensen et al. 2009), the presence of this pathogen on corncobs could represent a potential mycotoxin contamination risk to the human food or animal feed supply chains.