Molecular Pathogens 2024, Vol.15, No.2, 93-105 http://microbescipublisher.com/index.php/mp 94 This study analyzes current research on the integrated management of Fusarium and other fungal pathogens in maize, evaluating the efficacy of various control methods, including chemical, biological, and cultural practices. It also assesses the role of genetic resistance in mitigating fungal infections and mycotoxin contamination, identifies gaps in current research, and suggests areas for future investigation. By summarizing existing research findings, this study provides a scientific basis for effectively controlling these diseases. Understanding and integrating different control strategies is crucial for improving maize yield and quality. This not only reduces crop losses but also ensures food security and human health. 2 Overview of Fusariumand Other Fungal Pathogens Fusariumspecies are among the most significant fungal pathogens affecting maize, causing diseases such as ear rot, kernel rot, and stalk rot. These pathogens not only reduce crop yield and quality but also produce mycotoxins, which pose serious health risks to humans and animals (Nayaka et al., 2009; Czembor et al., 2014; Zhou et al., 2018). Other notable fungal pathogens in maize include species from the genera Aspergillus, Penicillium, and Cladosporium, which also contribute to crop losses and mycotoxin contamination (Munkvold, 2003; Czarnecka et al., 2022). 2.1 Common fungal pathogens in Maize Fusarium verticillioides, Fusarium proliferatum, and Fusarium graminearumare the primary Fusariumspecies causing ear and kernel rot in maize. These species are prevalent in various regions, including China, Poland, and Spain, and are known for their ability to produce harmful mycotoxins such as fumonisins and deoxynivalenol (DON) (Varela et al., 2013; Czembor et al., 2014; Zhou et al., 2018). Additionally, Fusarium temperatum has been identified as a significant pathogen in both Europe and China, causing ear rot and contributing to mycotoxin contamination (Varela et al., 2013; Czembor et al., 2014; Zhang et al., 2014). Other fungal pathogens include Fusarium oxysporum, Fusarium poae, and Fusarium sporotrichioides, which are frequently detected in maize fields, particularly in organic farming systems where chemical control is limited (Czarnecka et al., 2022). These pathogens, along with Alternaria alternata, contribute to the complex disease landscape in maize cultivation. 2.2 Symptoms and identification Fusariumear rot is characterized by the presence of white, pink, or salmon-colored mold on maize kernels, often accompanied by a "starburst" pattern of white streaks. Infected kernels may also exhibit discoloration and reduced size (Shang et al., 2020; Shang et al., 2022). Gibberella ear rot, caused by Fusariumgraminearum, presents as red or pink mold on the ear, often starting at the tip and progressing downwards (Munkvold, 2003). Stalk rot symptoms include the browning and softening of the stalk tissue, leading to plant lodging and reduced nutrient transport. Seedling blight, caused by Fusarium species such as F. temperatum, manifests as seedling malformations, chlorosis, and shoot reduction (Varela et al., 2013). Identification of these pathogens involves both morphological and molecular techniques. Morphological identification is based on colony characteristics, spore morphology, and growth patterns on specific media (Varela et al., 2013; Czembor et al., 2014). Molecular identification utilizes DNA sequencing of genes such as translation elongation factor 1-alpha (TEF-1α) and internal transcribed spacer (ITS) regions to accurately differentiate Fusariumspecies (Shang et al., 2020; Shang et al., 2022). 2.3 Life cycle and epidemiology Fusariumspecies have a complex life cycle that includes both sexual and asexual reproduction. The fungi produce conidia (asexual spores) that are dispersed by wind, rain, and insects, leading to infection of maize plants. The sexual stage, producing ascospores, occurs under specific environmental conditions and contributes to the genetic diversity of the pathogen population (Munkvold, 2003).
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