Wheat snow rot, also known as leaf blight and red snow rot, is a fungal disease that affects wheat from the germination stage through to maturity. The disease manifests in various forms, including bud rot, seedling drying, sheath rot, leaf drying, and ear rot. Among these, leaf blight and sheath rot are the most significant. During the early stages, bud rot and seedling infection lead to discoloration of radicles, radicle sheaths, and coleoptiles, resulting in fewer and shorter roots. On the coleoptile, dark brown, bar-shaped or oblong spots appear, often accompanied by severe rot and white hyphae on the surface.
The base of the leaf sheath becomes brown and necrotic, spreading upward and causing the entire leaf to turn brown or yellow and eventually die. Affected seedlings are weak, with underdeveloped or shortened roots and shortened first and second leaves. In severe cases, the entire plant may become waterlogged with brownish rot, leading to death and falling over, with white mycelium visible on the surface.
As the disease progresses, the infected basal parts of the pedicels move upward after jointing. The leaf sheaths of the lower nodes become brown and rotted, turning from dark brown to light yellow. The leaves connected to these sheaths may also become infected, turning brown and dying quickly. Sheath rot typically starts at the junction between the leaf sheath and blade, spreading toward the base of the leaf blade and the lower part of the sheath. The affected sheath turns yellowish or yellow-brown, with no clear boundary to the discolored area. High humidity can lead to sparse red mold growth.
Infected upper leaf sheaths can cause the flag leaf and next leaf to die. In adult plants, the initial symptoms on the leaves are water-soaked lesions that expand into oval or round spots, usually along the leaf margins. These spots range from 1 to 4 cm in size, with grayish edges and brown staining in the center. The infection spreads outward, forming distinct ring-like patterns. Brick-red molds are visible on the lesions. When humidity is high, a white hyphae layer appears around the lesion, and sometimes small black structures—ascospores—are present.
Spikelets may show black-brown patches on the glumes, with red mold and brown rot on the rachis. In severe cases, full ears may become yellow and shriveled, with grains easily wrinkling and turning brown, covered in white mycelium.
The pathogen responsible for this disease is *Gerlachia nivalis* (Ces. ex Sacc.) Gams and Mull., also known as *Fusarium nivale* (Fr.) Ces. It produces conidiophores on infected leaves, generating conidia that are crescent-shaped, colorless, and have 0–3 septa, mostly one. The sexual stage is *Monographella nivalis*, producing ascospores that are rod-shaped or cylindrical, ranging from 40–70 × 3.5–6.5 μm. Each ascus contains 6–8 ascospores, which are transparent, colorless, and have 1–3 compartments, measuring 10–18 × 3.6–4.5 μm.
The disease spreads when the pathogen overwinters on seeds, soil, and crop residues, then infects leaf sheaths and spreads to other parts, repeating infections. It thrives in temperatures between -2°C and 30°C, with an optimal range of 19–21°C. In regions like the northwest, where April and May bring high rainfall and low temperatures, conditions are favorable for disease development. Similarly, the Qinghai-Tibet Plateau experiences rainy July and August with cooler temperatures, increasing the risk of infection.
In addition to damaging leaves, the pathogen can cause ear rot. Wet, cool, and humid areas—especially mountainous regions and irrigated plains—are more prone to outbreaks. After the heading stage, prolonged rainfall increases the likelihood of infection. Freezing damage during jointing and booting stages can weaken the plant's resistance. Different wheat varieties show varying levels of resistance.
In spring wheat-growing areas, the disease typically peaks during the milk ripening stage. Management practices such as irrigation, fertilization, sowing time, and planting density significantly influence disease occurrence. Excessive spring irrigation, late nitrogen application, and high soil moisture increase susceptibility. Overly dense planting, early sowing, and excessive seeding rates also contribute to disease spread.
Control strategies include selecting resistant varieties like Zhengzhou No. 3, Huapei 28, Xiaojing No. 6, Zhoumai No. 10, Abo, Xinong 88, Xinong 881, Fengchan No. 3, and Qinmai No. 12. Using disease-free seeds is crucial. Timely sowing, proper planting density, and balanced fertilization help reduce risk. Avoiding excessive irrigation, especially in early spring, and using compost or organic fertilizers can improve field conditions.
In areas with high humidity, dense planting, or early infection, applying fungicides such as 80% carbendazim ultrafine powder (1000x), 36% Thiophanate suspension (500x), 50% Benomyl WP (1500x), or 25% Triadimefon EC (2000x) before and after winter can be effective. These measures help manage the disease and protect yield.
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