​Puccinia sorghi causes common rust to corn. It is a biotrophic fungus, only infecting and receiving nutrition from living cells. This fungus has a complicated life cycle like most rust fungi. Spores carried by wind to the surface of the corn leaves, germinate and produce a gelatinous coating that allows it to stick to the corn epidermis. The hyphae produce an appresorium above a stomate, from which it enters to leaf.  The hyphae then penetrate adjacent cells, absorbing nutrition while keeping the host cells alive. Within 7 days, the fungus produces new spores (urediniospores), from the pustule formed from the erupted epidermis.  These spores then are spread to more corn leaf tissue. As the host plant matures towards the end of the season, the fungus produces teliospores with diploid nuclei as the two nuclei in the former hyphae are joined.  Teliospores will germinate, undergo meiosis and form haploid basidiospores that cannot infect corn. Instead, the basidiospores germinate to form hyphae that fuse with hyphae of a compatible mating type, forming hyphae cells with the two nuclei.  These hyphae infect only the alternate hosts of the genus Oxalis species occurring in the tropics.  These infections result in production of a different type of spore called aeciospores that will infect corn.  Pustules on those corn plants produce the urediniospores that will spread to more corn.  This complicated life cycle easily occurs in tropics but corn in the USA and other temperate zones is produced by continuous corn crops in semitropical areas such as Mexico and Caribbean Islands.  Spring storms from those areas carries the urediniospores north to infect young corn crops from which the pathogen is spread to other fields.
 
Corn plants express two types of resistance to this fungus.  Rapid collapse of the infected cell essentially deprives the fungus of nutrition.  As many as 24 variants of 4 different single gene loci have been identified with this type of resistance.  When effective, no rust pustules are formed. Unfortunately, in most cases, races of the fungus have been found that overcome each of these single gene resistance methods. 
 
More stability in resistance that allows a few pustules to form is inherited by 3-5 genes and is effected by a more common phenomenon of detection of the pathogen, inducing the promotion of chemicals that inhibit further spread of the fungus.  Multigene resistance shows the typical pattern of detection of the pathogen and production of anti-pathogen chemicals effective of killing and/or limiting the sporulation of the pathogen.  Some of this may be common to other corn disease reactions.  We have seen the interaction of this general resistance for P. sorghi and the northern leaf blight fungus Exserohilum turcicum.  If spring storms bring in rust spores immediately before we artificially inoculate plants with E. turcicum, we see fewer northern leaf blight lesions than expected. The opposite has also been found by others (Phytopathology 106:745-751) in which inoculating the plants with E. turcicum before applying P. sorghi spores resulted in a reduction of formation of rust pustules.  This is consistent with the view that some portion of the quantitative resistance system to these two pathogens is shared in corn plants.
 
As usual, single gene resistance is easier to detect and breed but the more long-term stability of adequate resistance to Puccinia sorghi comes with multigene, quantitative resistance.

​Another smut-causing fungus is Sphacelotheca reiliana. This smut shows mostly in the complete destruction of the ear and the tassel of corn.  This species also attacks sorghum, Johnson grass and Teosinte.  The diploid teliospores of this fungus, shed from the smutted ears and tassel remain dormant in the soils for many years but when activated by the root exudates from susceptible corn seedling, the spore undergoes meiosis, producing short hyphae and then haploid basidiospores.  These spores germinate to form hyphae that fuse with compatible haploid hyphae, resulting the cells with two haploid nuclei.  From this point the fungus infects root cells, apparently growing between the cell wall and the cell membrane of the affected cell.
 
Absorbing the nutrients from the infected, live cell, the fungus continues growing cell to cell towards the meristems of the seedling.  From there It continues to advance without killing corn cells as they undergo cell division and eventually producing the ear and tassel.  Disease symptoms from the infection are absent as the fungus absorbs nutrients but does not kill tissue nor penetrate the cell membranes. 
 
After the host plant’s meristematic cells at the upper tip of the stalk and ear change to producing pollen mother cells and ovules, the fungal cells also change.  The two compatible nuclei in each fungal cell fuse to form diploid single cells.  These fungal diploid cells fill and destroy the host cells in the tassel and ears before pollination.  The individual, diploid fungal cells develop thick walls resulting in the first sign of the disease as a loose powder forms instead of ears on the corn plants.  These teliospores are then spread by the wind, the thick wall giving them survival until another host plant is found for repetition of the cycle.
 
Fortunately, high levels of resistance to head smut is more common than susceptibility.  Some of the resistance is thought to be from differences in the root exudates in the initial induction of teliospore germination.  Some comes from the successful recognition of the initial invasion, triggering the response by the host of producing enzymes to keep the pathogen from reaching the meristems. Perhaps it involves the speed of the plants cell divisions, escaping the fungus while infected cells produce anti-fungal chemistry.  Regardless of the method, most corn hybrids are reasonably resistant.
 
The problem historically has been with popular, susceptible hybrids being planted for consecutive years, allowing an increasing concentration of teliospores, until the right environment such as warm, light soils at time of corn seed germination results in noticeable high infection rate.  Switching to more resistant hybrids in future seasons reduces the occurrence of head smut.
 
Biology of corn includes the biology of pathogens. 

​Ustilago maydis, the cause of common smut of corn, has a complex life as it interacts with corn biology.  The dried galls in corn ears, tassels, or leaves include a powder composed of thousands of spores called teliospores.  These thick-walled spores, with a diploid nucleus are able to withstand many environments for many years on and in the soil.  When they germinate, on a corn plant, mitosis in the diploid nucleus creates short hyphal strands with haploid spores called basidiospores.  These spores germinate to produce short hyphal strands that fuse to form new hyphae with each cell containing the two haploid nuclei. These hyphae can form an appresorium on the leaf from which the fungus penetrates an epidermal cell.  This stage of the fungus is total biotrophic, receiving nutrition only from the living cells.
 
During the leaf stage of infection, the hyphae grow to surrounding cells, again invading and feeding on living cells.  As the nutrition is depleted, the two nuclei in the hyphae cells fuse to form a diploid and finally teliospores.
 
The fungus generally grows towards plant meristems.   These could be in those ear meristems located at each leaf node of the plant, resulting in the appearance of stalk smut galls but actually galls formed in those ear meristems that do not normally produce ears.
 
Infection is common in the silks of ears. Teliospores germinate, produce the haploid basidiospores, and short filaments on the silk.  These filaments fuse to form hyphae with the two haploid nuclei in each cell within the filament as they grow towards the ovule at the end of the silk.  Reaching the ovule, it invades to absorb the nutrients from the host cells, causing the cells to swell as it keeps the cells alive but absorbs the nutrients. It is during this time that the nuclei of U. maydis cells fuse to form diploids. Eventually these diploid cells develop the thick, walls of the teliospores, the tissue dries and teliospores spread in the wind.  These spores may remain dormant for several years until the next opportunity for infection of corn plants.
 
One of the functions of the abscission layer that develops at the attachment of the silk to the ovule after pollination is to stop intrusion of potential pathogens such as Ustilago maydis.  Consequently, infection of ears by this fungus is most frequent in poorly or delayed pollinated ear shoots.  Resistance to this disease includes good timing of pollen production and emergence of silks when the plant is under stress conditions.  Occurrence of the smut at the tips of ears suggests that poor pollination occurred at the end of the silking period.
 
Newly formed smut galls include both host plant material and fungus.  These fresh galls are relished as food in the Mexican culture.  Production of large quantities involves taking advantage of the host and pathogen biology, growing male sterile corn and spraying the silks with the teliospores saved from previous years. 
 

​Another fungus that has taken advantage of the minimum tillage practices is Colletrichum graminicola, the cause of anthracnose.  It is most aggressive on weakened plant tissue, causing lesions on seedling leaves during cloudy rainy periods, on senescing leaves and weakened stalks.
 
The fungus remains viable on dead corn leaves and stalks if tissue is exposed on soil surface.  Conidia are produced within a gelatinous material that protects them from dehydration. Spread by splashing water onto seedlings or spread by wind later in the season, these spores germinate when in water on plant material within 12 hrs. Within 24 hours, the hypha form appresoria from which penetration pegs grow into epidermal cells. These infected plant cells respond by producing fungal-inhibiting compounds including hydrogen peroxide. Before the resistance system takes full affect, the fungus keeps the cell alive as it absorbs nutrition from these cells. It then produces hyphal branches expanding into the areas between cells as it switches from existing within living cells (biotrophy) to killing tissue and producing enzymes to digest materials in dead plant tissue (necrotrophy).  This is probably common among corn leaf pathogens that can be called hemibiotrophic pathogens. This mode differs from the rust and smut fungi that are totally biotrophs, dependent solely on living cells
 
After receiving nutrition from the dead tissue, the C. graminicola produces a large number of conidia to spread to other areas.  Most corn hybrids have limited damage from the leaf infection phase from this hybrid.  I am aware of a hybrid in the 70’s that would commonly show many leaf lesions but continued to have good yields and stalk quality.  Others have verified that the leaf disease phase does not lead to the stalk infection phase.
 
Stalk infection by this fungus is confusing.  The fungus causes a black discoloration in the outer rind cells, making it easy to see.  However, inoculation of stalks with the fungus shows that it does not actively kill the stalk pith tissue except only when the tissue is already senescing. A study published in 1980 (Phytopathology 70:534) showed that reducing photosynthesis by removing leaves increased stalk rot from the Anthracnose fungus, just as it did from others such as Gibberella and Diplodia.  It appears that this fungus is basically held off by vigorous, living corn pith tissue but can destroy senescing tissue.  This accounts also for its appearance along with early death of the flag leaf.  The flow of carbohydrates to the kernels depletes sugars from pith tissue first from the upper and lower stalk.  The senescence in the pith in the upper internode allows Colletotrichum graminicola to gain momentum, resulting in black streaks in the rind beginning at the node of that internode.  As a result of the infection and the depletion of sugars the upper flag leaf dies.  Usually this occurs before death of the lower stalk but can signal a potential for eventual stalk rot in the plant if it is not near finishing normal kernel fill.
 
There are single genes available that can inhibit the anthracnose fungus from colonizing the stalk tissue but these do not affect any of the other fungi from inhabiting the stressed corn plant. The gene does not cause any significant reduction in occurrence of stalk rot but only less of it associated with anthracnose. 

​ An interesting discussion of corn and this pathogen can be found at Plant Physiol. 2012 Mar; 158(3): 1342–1358

​Another disease that seemed to suddenly appear on corn was eyespot when it showed up in Japan in 1956, the pathogen identified in 1959 as Kabatiella zeae (Aureobasidium zeae).    It was first identified in the USA in 1968 in Southern Wisconsin, Southern Minnesota and Michigan.  In 1971, it was found in New Zealand.  Later it was found Europe, Argentina and Brazil.  Studies indicate that its host range is limited to corn and its close relatives such as teosinte.  Where was it before 1956 and why did it suddenly appear in so many areas?
 
This fungus forms special hyphae in dry leaf tissue able to withstand winters if left above soil.  When the leaf tissue is moistened in temperatures above 51°F (11°C) this fungus produces conidia.  This allows Kabatiella zeae a competitive advantage over saprophytic fungi also occupying the dead leaf debris in the early part of cooler growing areas of corn.  Studies have shown that the more eyespot infected material remaining on the soil from the previous season the greater the number of eyespot lesions on young plants in the new season.  These infected leaves continue to produce spores for up to 60 days.
 
Initial infection of first 5-10 leaves become the inoculum source for spread to upper leaves within the corn field. Although the lesions are small (no larger than ¼ Inch (0.5 cm) in diameter, a large number of early lesions can provide a large load of inoculum to infect upper leaves, ultimately reducing photosynthesis.  This can trip the imbalance of carbohydrate supplies to roots that cause early plant wilt and stalk rot.
 
Most corn genotypes can be infected by this fungus but relatively few are extremely susceptible.  Resistance appears to involve a dominant gene and some minor genes.  Resistance is expressed by fewer lesions from initial infection and from later secondary infection.  So why the sudden appearance of this disease in the 50’s and 60’s?  In the USA, popular hybrids in the northern Midwestern corn belt had a very susceptible inbred W64A or W117 as one parent.  It also coincided with increased minimum tillage practices.  Recognition of the susceptibility led to the reduced use of the most susceptible hybrids but the other advantages of reduced tillage and lack of crop rotation has allowed this disease to persist.
 
Once again, inadvertent selection of susceptibility but successful general hybrid performance combined with agronomic change resulted in a new disease problem caused by a previously unknown corn pathogen. 

​Another surprise to corn was the emergence of the rare gray leaf spot disease in the 1970s.  It was mostly undetected after the initial description in 1925.  After outbreaks in the humid valleys of the eastern USA, I was among others who thought that was the primary environment for this disease.  Then it was found in Ohio River valley, then humid river bottoms in Iowa and then, by early 80s in Nebraska.  Combination of wide use of susceptible hybrids, including a few with extreme susceptibility and increased use of minimum tillage allowed proliferation of the fungus across the US corn belt.  Currently it is found in humid, warm corn areas of all continents.
 
Gray leaf spot is caused by the fungi Cercospora zeae-maydis and, occasionally, Cercospora zeina.  Most fungal corn leaf pathogens infect corn by spores germinating and penetrating the corn leaf within a few hours after exposure to moisture on the leaf surface. Spores of the gray leaf pathogens germinate on leaf surface but the hyphae grow on the surface of the leaf for a prolonged time that is mostly determined by the humidity.  The hyphal growth continues with 90-100% humidity and temporarily stopped when the air is drier.  After about 100 hours of the high humidity it establishes the flat bed (appresorium) over a stomata, from which it grows into the corn leaf.   Once inside the leaf, the fungus produces a toxin called cercosporin.  This toxin, activated by light, reacts with oxygen to produce a metabolite that damages cell membranes.  Leaked contents from the damaged cells serves as nutrition source for the fungus. The damage is restricted by the plant to areas between leaf vascular bundles, resulting in the diagnostic narrow, elongate lesions. Corn resistance is reflected in limiting the size of the lesions.
 
The fungus remains in the dead leaf tissue even after harvest but apparently does not compete well with other fungi if buried in soil.  Left on the soil surface, it produces spores (conidia) with warmth and moisture. spores easily distributed in the wind to begin the next cycle.   This could be a source of continued infection for much of the corn season.
 
Unexpected arrival and spread of this disease is another example of conflation of susceptibility of a widely used genetics (i.e. B73) and change in agronomic practice and a potential pathogen.  After acknowledging its potential damage, evaluations for resistance resulted in varieties with limited susceptibility and limited damage.

​Potential leaf pathogens of corn, feeding on bits of corn leaves or other grasses survive on ability to kill some plant tissue, dominate the dead tissue, produce large quantities of spores and spread to more live plant tissue.  The quantities of spores spread over large areas make analyses of their genetic diversity difficult because nearly any sampling system is insufficient.
 
Corn breeders can use methods to screen their new inbreds and hybrids for resistance to known variants of pathogens.  Resistance requires gene products that allow recognition of the pathogen invasion and quick response by production of pathogen-inhibiting substances by the adjacent plant cells.  Corn’s history, fueled by it cross-pollination biology and human’s transport to multiple environments has resulted in a large genetic diversity available to battle new pathogens. Problems arise with the unknown or unexpected pathogens.
 
Corn diversity also allowed selection of mitochondria with an unexpected fatal susceptibility to a race of Cochliobolus maydis, the accidental selection of the homozygous recessive gene allowing the damaging attack of race 1 of Cochliobolus carbonum.  The fungus Bipolaris turcicum did its genetic diversity part by including races of that avoided the corn Ht1, Ht2, Ht3 and HtN resistance mechanisms.
 
Multiple corn diseases have suddenly become significant in some corn growing area as the result of favoring pathogen genetics, susceptible corn defense genetics and environmental change favoring the pathogen.  With study and analysis, corn breeders have always been able to reach into corns genetic diversity to successfully limit the disease damage.
 
This battle in the cornfield will continue.

Most leaf pathogens have a means of destroying leaf tissue, creating a nutrition source before the host defense system limits their progress.  The invading fungus quickly dominates the dead tissue before saprophytic competitors arrive. From this base, they produce spores to invade new leaf areas.  Often the death to the tissue is related to production of a plant toxin affecting cell membranes. Bipolaris zeicola (Cochliobolus carbonum) and Bipolaris maydis (Cochliobolus maydis) share this mechanism.  These related species generally had limited success in destroying leaf tissue except when attacking a corn genotype that was particularly slow in stopping the infection.  Race 1 of B. zeicola is very damaging to inbreds with the homozygous recessive hm gene.  Race 2 of this pathogen can be notable on a few inbreds. 
 
B. maydis was known a problem on some inbreds and hybrids in the more southern USA and subtropical corn growing areas but generally adequate resistance was found.  This changed in 1969, when it was discovered that a variant of this pathogen produced a toxin attacking the unique membrane of mitochondria in T cytoplasm corn.  The unique mitochondria responsible for producing defective pollen grains, allowing cost saving in seed production, also resulted in extreme susceptibility to Race T of B. maydis.  Resistance to this pathogen race inherited via chromosomes had little effect on restricting this disease spread in 1970.  Use of T cytoplasm in corn throughout the USA, favorable weather and extreme pathogenicity of the new race allowed the spread of B. maydis into areas overlapping the normal distribution of B. zeicola.
 
Virtually all t cytoplasm corn had been removed from the market by the summer of 1972.  But lesions started were showing up on inbreds that were not as severe as race t on t cytoplasm but more vigorous than those caused traditional B. zeicola.  The fungal spores associated with these lesions varied in pigment and curvature from traditional B. zeicola or B. maydis.  It was known, experimentally, that the two species could cross.  It was thus easy to hypothesize that the widespread distribution and intensity of race T allowed many opportunities for the two species to cross and we were witnessing new segregating populations of the population.  No longer having the T cytoplasm to attack the new mix of pathogenic genes created new race possibilities.  One caused lone very narrow lesions on some inbreds that became known as Race 3 of Bipolaris zeicola.  Another pathotype (or race) was identified as causing more oval shaped lesions on some inbreds, especially with B73 background in 1990.  It was named B. zeicola pathotype 4.
 
Two related species apparently crossed in a strange coincidence of circumstances, new opportunities for new pathogen variants were created.  Biologies of corn and fungi often mix in the real world of agriculture.