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Southern corn leaf blight

Southern corn leaf blight (SCLB) is a destructive foliar of (Zea mays) caused by the ascomycete Bipolaris maydis (teleomorph Cochliobolus heterostrophus), which produces tan to brown lesions on leaves that restrict and can lead to severe yield reductions of up to 50% or more under favorable conditions. The exists in multiple races, including Race O (which primarily affects leaves) and Race T (which can infect leaves, stalks, ears, and kernels, especially in susceptible cytoplasmic male-sterile lines), with optimal growth occurring in warm, humid environments at temperatures around 30°C. The disease gained notoriety during the 1970–1971 epidemic in the United States, where Race T exploited the widespread use of Texas cytoplasmic male sterility (cms-T) in approximately 85% of commercial hybrids, resulting in the loss of about 710 million bushels—equivalent to 16% of the national and roughly $ in (over $8 billion in today's dollars). This outbreak, which originated from a first identified in the in 1961 and spread to the U.S. by 1969, underscored the risks of genetic uniformity in modern agriculture and prompted a rapid shift away from cms-T lines toward fertile and methods for production. Today, SCLB remains a concern in tropical and subtropical regions with high humidity, where it spreads via wind-borne conidia and persists in crop residues or soil, though its impact has been mitigated through breeding for resistance—such as the incorporation of genes like rhm1 for Race O tolerance—and integrated management practices including , timely applications, and field . The epidemic's legacy continues to inform strategies for surveillance and in crop production, emphasizing the need for ongoing public-private collaboration to prevent similar vulnerabilities.

Pathogen

Causal Organism

Southern corn leaf blight is caused by the ascomycetous Bipolaris maydis (anamorph), whose teleomorph is Cochliobolus heterostrophus. This belongs to the phylum , class , order Pleosporales, and family Pleosporaceae. The was first described in as Helminthosporium maydis by Nisikado and Miyake in 1926, based on specimens from diseased leaves. The teleomorph was originally described as Ophiobolus heterostrophus by Drechsler in 1925 and later transferred to Cochliobolus heterostrophus in 1934. In 1959, advances in fungal led to the reclassification of the anamorph from Helminthosporium to Bipolaris by Shoemaker based on conidial morphology and septation patterns, with further confirmation through molecular phylogenetic analyses in subsequent decades. Morphologically, B. maydis produces conidia that are typically curved or canoe-shaped to fusoid or obclavate, with 3–14 distoseptate walls (usually more than 6 ), pale to deep olivaceous or reddish-brown pigmentation, and dimensions of 60–140 × 11–18 μm; these conidia germinate via 1–2 polar germ tubes from a slightly protruding or truncate hilum. The sexual ascospores, produced rarely in the teleomorph stage, are filiform or flagelliform, to pale yellow-brown at maturity, multi-septate, and helically coiled within the asci, often surrounded by a mucilaginous . C. heterostrophus exhibits a , beginning with an initial biotrophic phase of intracellular without immediate , followed by a switch to necrotrophy where it actively kills and feeds on necrotic tissue. This pathogen produces non-host-specific metabolites and, in certain races like Race T, host-specific T-toxin, a linear that disrupts mitochondrial function in susceptible cytoplasm, enhancing disease severity.

Races of the Pathogen

The pathogen Bipolaris maydis (teleomorph Cochliobolus heterostrophus) exists in three physiological races—O, T, and C—differentiated by their host specificity and factors, particularly their ability to produce host-selective toxins that target specific (CMS) types. These races share core genetic elements but differ in pathogenicity loci that confer on distinct genotypes. Race O is the most prevalent race worldwide, exhibiting low virulence primarily on with normal (N) cytoplasm and lacking production of host-specific toxins, relying instead on non-specific mechanisms for . It causes typical foliar lesions but does not aggressively infect CMS lines, making it less destructive compared to the other races. Its global distribution reflects adaptation to diverse maize varieties without CMS vulnerabilities. Race T, identified as a mutation in 1969, demonstrates high virulence specifically on Texas CMS (T-cms) through production of the host-selective T-toxin, which disrupts mitochondrial function in susceptible plants. This race triggered the devastating in the United States, where approximately 85% of commercial hybrids carried T-cms, resulting in about 16% crop loss nationwide. The T-toxin enables rapid lesion expansion on leaves, sheaths, and ears of T-cms hosts, but Race T shows virulence similar to Race O on normal . Race C is virulent exclusively on Chinese CMS (C-cms) maize, primarily in Asia, where it produces a C-toxin analogous to T-toxin but targeting distinct mitochondrial components in C-cms plants, leading to enhanced leakage and tissue . Unlike Race T, it does not affect T-cms lines and remains geographically limited, with no major epidemics reported outside . The genetic basis of these races involves pathogenicity genes located on supernumerary (dispensable) chromosomes, which are absent or inactive in Race O. For Race T, the T-toxin biosynthesis pathway is encoded by the TOX1 locus, a ~1.3 Mb region containing over 20 genes, including polyketide synthases and accessory enzymes, that assemble the linear polyketol ; this locus arose via and is conditionally dispensable, present only in virulent strains. Similar genetic architecture underlies C-toxin production in Race C, though specific genes differ in targeting C-cms mitochondria. Detection of races relies on molecular markers, such as amplification of TOX1-specific genes to distinguish Race T from Race O, or toxin bioassays on differential lines; species-specific primers targeting the (ITS) region further confirm B. maydis identity before race typing. These methods enable rapid field surveillance without reliance on symptomatic differentials.

Hosts and Symptoms

Host Range

The primary host of the fungal pathogen Bipolaris maydis, which causes southern corn leaf blight, is Zea mays ( or corn), affecting plants at all growth stages but causing the most severe damage when infections occur on leaves prior to tasseling, as this period coincides with peak photosynthetic activity essential for grain fill. Alternative hosts include Sorghum bicolor (sorghum), teosinte (Zea luxurians), and certain wild grasses, though infections on these non-corn species typically do not result in economically significant losses. Susceptibility in maize varies by cytoplasmic male sterility (CMS) types and pathogen race: varieties with Texas CMS (T-cms) cytoplasm are highly vulnerable to Race T of B. maydis due to sensitivity to its T-toxin, whereas those with normal (N) cytoplasm exhibit resistance to Race T but remain susceptible to Race O. Most dicotyledonous plants and cool-season cereals such as wheat serve as non-hosts, with no evidence of transmission to humans or animals.

Disease Symptoms

Southern corn leaf blight manifests initially as small, tan to gray lesions on the lower leaves of infected corn plants, typically measuring 0.25 to 1 inch (0.6 to 2.5 cm) in length and 0.125 to 0.25 inch (0.3 to 0.6 cm) in width. These lesions are often diamond- or spindle-shaped with buff-colored centers and may be bordered by reddish-brown or purplish margins, depending on the host genotype. In infections caused by Race O of the pathogen Bipolaris maydis, the lesions are typically 3–22 mm long and 2–6 mm wide, and less numerous compared to Race T. As the disease progresses, the lesions enlarge and coalesce, often covering more than 50% of the leaf surface and leading to widespread blighting. In advanced stages, particularly with Race T, rapid causes the leaves to develop a shredded appearance, with extensive tissue death between lesions. Race T infections also extend to stalks, causing and rot, and to ears, resulting in pinkish mold on the kernels that promotes ear rot. At the level, severe lead to premature and death of leaves, reduced , stalk , and the production of barren or poorly filled ears. These effects can result in yield losses of up to 50% or more in severe cases, with localized impacts reaching 70% in highly susceptible varieties during epidemics. Symptoms typically appear 7 to 14 days after and intensify under humid conditions that favor . Southern corn leaf blight can be differentiated from similar diseases like northern corn leaf blight by its smaller, tan to gray lesions with defined borders, in contrast to the larger (3-9 cm), cigar-shaped, gray-green lesions of the latter.

Disease Development

Life Cycle

The life cycle of Bipolaris maydis, the causal agent of southern corn leaf blight, is predominantly and polycyclic, enabling multiple generations within a single growing season. Conidia, the primary infectious propagules, are dispersed by wind or rain splash onto susceptible corn surfaces, where they germinate under moist conditions, producing polar germ tubes that form appressoria for penetration either directly through the or via stomata or wounds. This and initial penetration typically occur within 6-12 hours in the presence of free water on the surface. Following penetration, an of 7-14 days ensues before visible lesions appear, during which the colonizes internally. Asexual reproduction dominates the cycle, with conidiation occurring on mature lesions under high humidity, where conidiophores emerge from stomata to produce chains of multicellular conidia that serve as secondary inoculum for further infections. This process allows the pathogen to complete a full cycle from infection to new spore production in as little as 60-72 hours under optimal warm, humid conditions, facilitating up to 5-10 generations per season in favorable environments. The sexual cycle, involving the teleomorph Cochliobolus heterostrophus, is rare and occurs primarily on overwintered debris, where compatible mating types form pseudothecia containing asci and ascospores; these ascospores can initiate new infections but play a minor role compared to asexual conidia. Overwintering primarily happens as and conidia within corn residue left on or incorporated into the soil surface, with viability persisting for 1-2 years depending on environmental conditions and practices; seed transmission occurs for both races, but is more prevalent in race T, with race O showing low infection rates. The lacks a distinct soilborne phase, relying instead on crop debris for survival between seasons. Sporulation and disease progression are optimized at temperatures of 24-30°C, with high relative (>90%) essential for conidial and expansion.

Environmental Influences

Southern corn leaf blight (SCLB) development is highly dependent on , with optimal conditions for , , and sporulation occurring between 20°C and 32°C (68°F to 90°F). Disease progression slows significantly below 15°C (60°F) or above 32°C, where fungal activity becomes minimal. These temperature ranges align with warm, humid growing seasons typical in maize-producing regions, where prolonged exposure during vegetative stages can accelerate formation and spread. Humidity and leaf moisture are critical drivers of SCLB initiation and progression, requiring periods of leaf wetness exceeding 6 hours for spore germination and penetration. High relative above 90% further promotes expansion and secondary sporulation by maintaining favorable microclimates on leaf surfaces. Weather events such as rainfall or provide the necessary free , often triggering outbreaks in susceptible fields. Other environmental factors, including planting density and management, influence severity by altering canopy microclimates. Dense planting configurations increase intra-canopy humidity, creating conditions conducive to prolonged leaf wetness and enhanced dispersal. While soil type has little direct impact on this foliar , retaining can elevate local humidity levels, potentially intensifying infections if not managed to improve air circulation. Under projected scenarios, wetter conditions may increase the risk and severity of SCLB outbreaks.

Spread and Survival

The primary dispersal of Bipolaris maydis conidia, the spores responsible for southern corn leaf blight, occurs via , allowing transport over long distances under favorable conditions. splash contributes to short-range spread, typically less than 1 m between , particularly in dense canopies during wet weather. No confirmed insect vectors facilitate transmission, distinguishing this pathogen from others that rely on assistance. Secondary spread is primarily driven by the movement of infected plant debris through agricultural practices such as , harvesting, or equipment transport, which can redistribute residue across fields or farms. Seed transmission plays a negligible role, particularly in commercially produced mature, dried seeds, rendering it an insignificant pathway for long-distance introduction. These mechanisms underscore the pathogen's reliance on local environmental factors rather than human-mediated long-range transport. For long-term persistence, B. maydis overwinters primarily as and conidia embedded in corn residue on or near the surface, with viability declining over seasons due to microbial and environmental . The sexual , involving pseudothecia that produce ascospores, occurs rarely and contributes minimally to survival compared to the dominant cycle. This residue-based overwintering highlights the importance of residue management in breaking disease cycles. Key sources of initial inoculum include volunteer corn plants emerging from unharvested kernels, which harbor viable spores and sustain local infections into the next growing season. Alternative hosts, such as certain grasses or weeds, provide limited contributions to inoculum buildup, as B. maydis exhibits strong host specificity toward maize.

Geographic Distribution

Southern corn leaf blight, caused by the fungus Bipolaris maydis, is distributed worldwide in maize-growing regions, with the highest prevalence in tropical and subtropical areas characterized by warm temperatures (20–32°C) and high humidity. It occurs across Asia, Africa, North and South America, the Caribbean, Europe, and Oceania, particularly in environments favoring fungal development during the growing season. While the disease is endemic to these humid subtropics, it appears sporadically in temperate zones where conditions occasionally align with pathogen requirements. In the United States, the disease was first reported in 1923 and remained a minor issue until the 1970 epidemic, when it severely affected the , spreading rapidly from southern states like and northward. Post-1970, incidence declined significantly in the due to the shift to hybrids with normal (fertile) cytoplasm, which are resistant to Race T, reducing its impact to low levels nationwide. However, outbreaks persist in humid southeastern states during favorable weather, such as in , , and , where the pathogen exploits susceptible varieties in wet conditions. Sporadic detections have also occurred in northern states like , as seen in 2018 on . Globally, high-incidence hotspots include maize-dependent tropical regions such as , , and , where the disease causes substantial foliar damage in intensive production systems. In , particularly sub-Saharan countries, southern corn leaf blight threatens maize yields alongside other foliar diseases, with potential increases linked to shifting climate patterns that extend humid periods. Race C of the pathogen remains confined to , distinguishing it from the more widespread Race O. Historical shifts reflect pre-1970 minor status in many areas, followed by post-epidemic management successes in the through hybrid breeding, though emerging risks in highlight ongoing vulnerabilities. Monitoring efforts, such as those by the USDA and international networks like CIMMYT, track incidence through field surveys and reports to inform integrated pest management, though formal quarantine measures are rarely applied due to the pathogen's widespread nature.

Management

Resistance Breeding

Following the 1970 epidemic, maize breeders rapidly transitioned from Texas male-sterile cytoplasm (T-cms) hybrids, which were highly susceptible to race T of Bipolaris maydis, to normal cytoplasm varieties that confer complete resistance to this race, effectively controlling the disease in temperate regions. This shift, completed within a few years, incorporated diverse germplasm sources, including exotic lines from Mexico through programs like the Germplasm Enhancement of Maize (GEM), to broaden the genetic base and enhance partial resistance to race O. Resistance to race O, the predominant pathotype in tropical and subtropical areas, is primarily partial and polygenic, governed by multiple quantitative trait loci (QTLs) identified across the , with notable clusters on chromosomes 2, 3, and 6 that collectively reduce size and sporulation. Key sources of this include diverse inbred lines such as Mo17, which exhibits moderate , in contrast to susceptible lines like B73; recombinant inbred populations derived from B73 × Mo17 have been instrumental in mapping these QTLs. A major gene, rhm1 on , provides recessive chlorotic- to race O and has been fine-mapped for use in breeding. Breeding strategies emphasize (MAS) with (SNP) markers linked to key resistance loci, enabling efficient pyramiding of QTLs from tropical into elite temperate hybrids without significant linkage drag. Modern approaches include CRISPR-Cas9 editing to enhance , such as knockout of the susceptibility ChSK1 (a receptor ), which confers strong to southern leaf blight in edited lines. Recent advances (as of 2025) have identified additional modules, including the ZmCPK39–ZmDi19–ZmPR10 immune pathway that regulates against B. maydis, and the ZmH2B involved in response to , providing new targets for durable breeding. Resistant varieties have reduced disease severity by 50-90% under field conditions, particularly for race T, though ongoing breeding efforts focus on race O in tropical environments where partial alone is insufficient against evolving populations.

Cultural and Chemical Controls

Cultural practices play a key role in suppressing Southern corn leaf blight (SCLB) by reducing inoculum and creating less favorable conditions for development. with non-host crops such as soybeans for at least one year, with longer rotations of 2-3 years providing additional benefits, helps break the cycle by limiting the survival of Bipolaris maydis on corn residue. Thorough , such as conventional or moldboard plowing, incorporates and buries crop debris, accelerating and reducing overwintering inoculum levels compared to no-till systems. Additionally, wider row spacings (e.g., 36 inches) promote better airflow within the canopy, decreasing and slowing lesion spread. Planting strategies further minimize SCLB risk by timing crop growth to evade peak environmental conditions conducive to . Early planting allows corn to reach reproductive stages before mid-summer peaks, reducing exposure to optimal conditions (temperatures of 25-30°C and high relative ). Avoiding dense stands, with populations limited to below 30,000 per , prevents excessive canopy closure that traps moisture and favors disease progression. Chemical controls involve foliar fungicide applications targeted at susceptible hybrids under high disease pressure. Effective options include strobilurins like (Group 11) and demethylation inhibitors like (Group 3), which provide very good to fair control of SCLB when applied preventatively. Applications are recommended from the V8 growth stage through tasseling, ideally 14-21 days before silking (VT-R1), with 1-2 treatments spaced 10-14 days apart to cover the critical period; these can significantly reduce lesion severity and preserve yield potential. Integrated pest management (IPM) combines these approaches for sustainable suppression. Regular scouting starting at V6, focusing on lower leaves for early lesions, is essential; for susceptible hybrids under conditions favoring spread (e.g., prolonged leaf wetness >12 hours), consider application when is present on upper leaves. IPM emphasizes hybrid susceptibility and environmental factors alongside cultural practices to optimize use and avoid unnecessary applications. Limitations to these controls include the potential for resistance, particularly in QoI (strobilurin) classes, though Bipolaris maydis remains sensitive in most regions as of 2024; rotating modes of is advised to mitigate this risk. Environmental regulations in some areas restrict use due to concerns over runoff and non-target impacts, making cultural methods preferable where feasible. Overall, while effective, chemical controls are rarely economical without integrated strategies, especially given variable disease pressure.

Historical and Economic Importance

The 1970 Epidemic

In the late 1960s, approximately 85% of U.S. corn hybrids relied on male-sterile (T-cms) for efficient production, creating widespread genetic vulnerability to certain pathogens. A virulent new strain, known as race T of Cochliobolus heterostrophus (formerly Helminthosporium maydis), originating from a first identified in the in 1961, first appeared in the United States in in 1969, capable of producing a that specifically targeted T-cms corn. This race T pathogen rapidly evolved, likely facilitated by supernumerary chromosomes that enhanced its virulence and spread. The epidemic began in in southern states, with initial reports in from Florida's Belle Glade area, where heavy infestations damaged corn fields. By May, the disease had intensified in , , , and other southern regions, spreading northward through wind, rain, and infected debris during a humid summer that favored fungal growth. It progressed rapidly, reaching the by July and extending as far north as and by September, with the most severe losses in and , where yields dropped by up to 50% in affected fields. Nationally, the outbreak reduced corn yields by about 15%, equivalent to a loss of 710 million bushels. The primary causes included the uniform susceptibility of T-cms hybrids to race T's toxin, which not only blighted leaves but also rotted stalks, ears, and kernels, compounded by the pathogen's quick adaptation and the unusually wet, warm weather across the U.S. . This combination allowed the disease to escalate from a minor issue—historically causing less than 1% annual loss—to a devastating event in a single season. Immediate economic impacts were profound, with total losses estimated at $1 billion in 1970 dollars (approximately $8.3 billion as of 2025), marking the largest single-season damage from a plant disease on a U.S. row crop. The shortage triggered spikes in corn and food prices, strained export reserves, and disrupted livestock feed supplies, though national grain stockpiles mitigated broader shortages. In response, researchers like A.L. Hooker, D.R. Smith, and S.M. Lim quickly identified normal cytoplasm sources of resistance in spring 1970. The USDA and seed companies launched emergency breeding programs, ramping up production of resistant hybrids in South America and Hawaii; by 1971, about 50% of U.S. seed was in normal cytoplasm, fully resolving the vulnerability by 1972.

Current Impact and Lessons

In the United States, southern corn leaf blight (SCLB) now causes minimal yield losses, typically less than 1%, due to the widespread adoption of resistant maize hybrids following the 1970 epidemic. In contrast, the disease remains a significant threat in tropical and subtropical regions of developing countries, where humid conditions favor its spread; yield losses can reach 20-30% in susceptible varieties, particularly in and . Globally, these impacts contribute to substantial economic costs, with potential annual losses exceeding hundreds of millions of dollars in affected areas, though precise figures vary by region and year. While trade restrictions due to SCLB are rare, outbreaks in climate-vulnerable can disrupt local food security and prompt insurance claims during unusually humid seasons. The 1970 epidemic underscored the dangers of genetic uniformity in systems, as the near-universal use of Texas male sterile cytoplasm (cms-T) in U.S. hybrids amplified vulnerability to a novel race, leading to 15% national yield loss. Key lessons include the critical need for diverse to buffer against such risks, as preserved genetic resources enabled rapid development of resistant varieties post-. Ongoing surveillance programs, such as those supported by the International and Improvement Center (CIMMYT), emphasize early detection of variants through global monitoring, as initial warnings from the in the 1960s highlighted the value of international collaboration. Looking ahead, poses future risks by potentially expanding SCLB's range through warmer, wetter conditions that enhance pathogen survival and dispersal, increasing outbreak probabilities in vulnerable regions. Emerging biotech solutions offer promising avenues for durable without relying solely on chemical controls. As an exemplar of epidemics—paralleling wheat stem rust outbreaks—SCLB has influenced agricultural policy toward greater , promoting diversified planting and conservation to mitigate vulnerabilities.

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