Corn breeders strive to produce inbreds that are homozygous, mostly to allow repeatable increase of the parents of hybrids and therefore making the identical hybrid plants each season.  Inbreeding causes both sets of each gene to be identical, whether it is a recessive or a dominant gene, ultimately causing the inbred parents of a hybrid to be much smaller than the hybrid.  Successful hybrids have favorable genes in one parent covering up the unfavorable ones of the other parent.  This is not only true of major agronomic characters but often susceptibility in one parent to a pathogen is modified in the hybrid by the resistance in the other parent.
 
Seed producers occasionally have problems in seed fields related to extreme susceptibility of one parent that can be severely damaging.  A common pathogen of corn and other grasses is the species Bipolaris zeicola (formerly known as Helminthosporium carbonum).  A variant of this fungus, known as race 1, produces a toxin that overcomes other resistance factors that corn produces to limit the pathogen.  This toxin is destroyed by corn plant cells that have the dominant version of the Hm1 gene, because this gene results in production of the right enzyme to do the job.  The problem comes when an inbred is homozygous recessive for the hm1 gene.
 
Such a case was found in seed fields in South Dakota, Illinois and Ohio in 2014 when a susceptible inbred was exposed to the race 1 of this fungus.  How did this inbred get through the system to the point it was in seed fields?  Traditional breeding methods in which an original segregating breeding population is selfed, then grown ear to row, from which individual selections are selfed again until 7-8 generations later the inbred was considered homozygous also meant that each generation it was grown, and selections were made.  I recall seeing one row of one of those selections heavily diseased by this pathogen as it and its sisters were being evaluated in a nursery in Nebraska 25 years ago.  That system was slow in developing new inbreds but it did allow for selections such as against normally minor traits, such as caused by hm1/hm1.  Haploid-dihaploid breeding has many advantages in quickly producing new inbreds but it is possible that those with the rare homozygous recessive gene for susceptibility to race 1 of Bipolaris zeicola would not be caught until the wider exposure in the seed fields.  Widespread testing of hybrids made from the susceptible parent would not show the problem because it is likely the other parent would have the dominant gene producing the anti-toxin enzyme.  The distribution of race 1 apparently is widespread, probably maintained on grasses and only revealed when the susceptible inbred is exposed to it.

The recent issue of Plant Disease http://apsjournals.apsnet.org/toc/pdis/100/4 includes studies of Goss’ wilt that illustrates how new distributions of corn diseases occurs. There are three studies published in that issue that do advance our knowledge of this disease but one, http://apsjournals.apsnet.org/doi/full/10.1094/PDIS-04-15-0486-RE , typifies the difficulty of detecting or predicting new problems.  Susceptible and resistant hybrids were planted in ground that had not been in corn during previous years.  There were three treatments: (1) plants inoculated after plant tissue was injured with a strain of the Goss bacteria that could be identified as distinct from the wild type, (2) Plants not inoculated but seedlings surrounded with dried leaf tissue infected with Goss from the previous year and (3) non-inoculated plants with no infected debris.
 
All of the wounded, inoculated plants on the susceptible hybrid showed typical symptoms by midseason. A few of the residue infected plants showed symptoms and even a few of the non-inoculated,  non-residue plants had symptoms.  That is consistent with my observations in our Goss inoculation field trials in which there would be a few plants near the inoculated plants that would show symptoms.  This disease is so closely linked to fields damaged by hail that I think we assumed that this was the only method of infection.  I hypothesized that insects may have carried the bacteria but another paper, http://apsjournals.apsnet.org/doi/full/10.1094/PDIS-08-15-0923-RE , by the same authors offers that infection could be occurring through open stomata or hydathodes near the margins of leaves.
 
This research supports the concept that a disease is not actually new by the time it is discovered. It arrives in a field through seed or wind or transitions from another grass to a corn variety previously unknown to be susceptible and slowly increases until it's noticed.  Good that we have many hybrid genetics available, that we have plant pathologists to try to figure out these dynamics and that we have people looking closely at our crop while it is growing.
 
 

Most ‘new’ corn diseases are not really new.  Instead they often are newly acknowledged in a country or a state.  Some are like Goss’s bacterial wilt, which is caused by a variant of pathogen (Clavibacter michiganensis subspecies nebraskensis) that was known to infect wheat and other grasses including foxtail, but,  in 1969 it was found to badly damage corn.  It caused severe losses to specific hybrids that had been damaged by hail previous to flowering.  It is probably significant that these fields were in an area of Nebraska where there was continuous corn cropping, often with the same popular genetics, and frequent early season hailstorms.  The extreme susceptibility seemed to be limited to relatively few corn parent inbreds.  Later the disease was found further east and most recently caused alarm, again with relatively few susceptible hybrids. This is one disease that seems to have originated from the combination of pathogen diversity, inadvertent inclusion of genetic susceptibility in host and perhaps continuous corn planting.
 
Head smut of corn, caused by a variant of the fungus Sphacelotheca reiliana, has showed up sporadically in many scattered areas in many countries.  The species is more common on sorghum and Sudan grass but the variant attacking corn is specific to corn.  Initial infection occurs in seedlings in relatively dry, sandy soils when initially planted at warmer temperatures than usual (70°F).    The fungus then grows within the plant towards the growing points as the plant develops, ultimately completely replacing the ear and the tassel with spores.  These thick-walled spores can remain viable in the soil for many years.  Although only a few plants initially are infected, the numbers increase over seasons, especially with susceptible hybrids, until it noticed and then appropriate changes are made.  How did it first get there? Maybe wind or perhaps carried by a few seed but it probably initially was so insignificant that no one noticed.  Head smut is not the same as common smut although both cause black spores.  Microscopic examination can distinguish between them. A field tip is that when head smut fungus shows up on the tassel there is nearly always an infected ear with no kernels.
 
We move seed and grain around the world and probably potential pathogens in very low rates move also.  Most corn pathogens also infect other grasses near our cornfields.  Genetic variation in the potential pathogens allow adaptation to corn.  Genetic variation in corn, contributing to the continual increase in performance, also allows for undetected genes for susceptibility to unsuspected pathogen.  By the time we see the ‘new’ disease, it probably has been present for a few years.  Takes a few more years to understand the dynamics but ultimately a combination of effort by many gets the disease under control.
 

Two corn diseases were reported in 2015 as basically new to USA Midwest.  Tar spot, reported in Illinois and Indiana is caused by a fungus, Phyllachora maydis and is known from its occurrence in Mexico.  The other one called bacterial leaf stripe, caused by Burkholdia andropogonis, was noted in the 70’s in Nebraska.  Neither disease appeared to be damaging but were noticeable enough to be sent to State Extension Pathologists for identity.  Physoderma brown spot also was more easily found last summer in the Midwest than the past many years. 
 
When new diseases are first found there is a good chance that they were present previously but not noticed at least by the right people to realize it was significant.  Large fields, many acres per farm operation, high plant densities make it obvious that only a few infected plants will go unseen.  But this is a reminder of the importance of getting diagnosis done by experts that have the knowledge and methods to give an accurate identification.
 
One of the most important roles for plant pathologists working for a company or government institution is to access the significance of a new occurrence of a disease.  Was it because of a change in weather, crop culture practice, host genetics or pathogen genetics?  Is it a future threat that needs to be addressed or simply a rare, non-damaging occurrence? 
 
Within my 45 years of working with corn diseases we have seen several ‘new’ diseases.  I initially thought gray leaf spot would remain mostly in the valleys of North Carolina and perhaps in humid areas along rivers.  Missed that one as it turned out that the fungus enjoyed some of the newer genetics of the late 70’s and general humidity of the Midwest including those irrigated fields in western corn belt.  When Corn Lethal Necrosis was first seen in Nebraska and realized that one of the viruses was transmitted by corn root worm beetles and the other virus was either wheat streak virus vectored by the wheat curl mite or sugar cane virus that virtually gets spread throughout the corn belt later in the season by aphids, I thought the disease would spread.  I won’t confess to all of my errant predictions but only state that it is really difficult to understand all the variables involved when an unexpected occurrence of a disease first is present.
 
It is very important that everyone is aware when seeing unusual symptoms that they get reported to experts, including the seed producer and corn pathologists.  A corn disease working group composed of state, federal and private company corn pathologists meet annually to discuss diseases noted the previous year as they attempt to predict significance.

 With the primary root growing below the seed and the first node of the stem (mesocotyl) pushing the coleoptile towards the light, vulnerabilities to infection by fungi becomes evident.  Eventually, the stem will produce new roots but until then the mesocotyl is essential to transport of the stored carbohydrates from the endosperm and minerals from the primary roots.  This is all occurring in the environment teeming with organisms dependent upon organic food sources.
 
Soil temperature and moisture plays a big role in the interactions between the corn physiology and the fungus activity.  Low temperatures lengthen the time of exposure of the germinating seed and at the same time favor fungi such as Pythium species.  Warmer temperatures favor rapid emergence and reduce the dependence upon the mesocotyl and primary root systems.  Warmth also increases the metabolic rate in the plant tissue that should improve the plants response to invasion by pathogens. 
 
Significance of fungal invasion of the mesocotyl is somewhat confusing, partly because of the complexity of studying seedling development in soils.  Fungi associated with seedling death such as Pythium species and Fusarium verticilliodesas as well as those involved in diseases that develop much later in the plant life such as Diplodia stalk rot or Head smut have been thought to initially invade the mesocotyl.
 
Corn genetics vary for resistance to these organisms and response to temperatures.  Seed germination quality varies with genetics, seed production environments, planting depth and soil conditions.  The fungi also are affected by their own genetics and environmental factors include temperature, moisture, previous crop and organic matter in the soil.  It is to the credit of everyone involved that we usually get the stands that we desire.

The mature embryo in a corn seed includes the cells already programmed to become the first 5 or 6 leaves, the primary root and a few secondary roots as well.  The cotyledon of this monocot is called the scutellum. This is the large white portion of the seed that remains attached to the endosperm and becomes the main conduit of energy for germination.
 
Imbibition, and sufficient heat energy, initiates germination which is mostly a process of cell elongation in the root and shoot areas of the embryo.  Root tip cells are surrounded by a special layer of cells (coleorhiza) that act as a protective covering when the root tissue, also called the radical, pushes through the pericarp of the seed.  At the other end of the embryo, a coleoptile protects the shoot tissue all the way to emergence from the soil.  This becomes the ‘spike’ that we first see in the field.
 
Root tips include special cells with organelles (statoliths) that are heavier than other parts of the cell.  Consequently, they accumulate on down side of the outer layer cells of root tissue.  These cells lead to production of hormone-like chemicals (auxins) that inhibit root cell elongation on the lower side of the emerging root.  With greater cell length on the upper side, the root grows downwards, regardless of the orientation of the seed when planted.
 
Shoot tips cells also produce similar organelles also affected by gravity.  They also produce auxins but these hormones have the opposite affect on shoot cell elongation.  Those cells on the gravity side with more auxin become longer than those on the upper side.  Consequently the shoot grows upwards.
 
Affect of gravity on plant growth direction is called geotropism.  After shoots emerge, phototropism becomes dominant, causing the plant to grow towards light because cells on the shaded side produce more auxin and consequently longer cells.

40 years ago, when pursuing the question of why one plant died early with stalk rot and the adjacent plant did not, I hypothesized that the dead plant was that one emerged late as a seedling.  When most of the plants in the test plots showed their 5th leaf, a tag was put near those that had only 3 leaves and another marking those with only a spike.  Notes were taken of these plants and their adjacent plant during the season.  At pollination, it was clear that even those tagged at three leaves were not silking in time with adjacent plants and tended to have more slender stalks. Many of those tagged as spiking no longer were present, but those that survived were far off in pollination timing, had very small, narrow stalks and, eventually, small tassels.  Ears were harvested at end of season and kernel numbers were counted. Those tagged with three leaves had only 20% of kernels of adjacent plants and those tagged as spike only were barren.  Delayed emerging plants did not develop stalk rot but clearly the delay affected yield.
 
To eliminate the possibility that these delayed plants were not ‘selfed’ inbreds instead of hybrid plants, an experiment was performed the next season to confirm that emergence delay was the main factor.  Seed was planted with twice the normal plant-to-plant spacing. When those seedlings spiked, the same hybrid seed was planted between the seedlings.   This would be an unusual delay but the effect was the same as the first observation.  Barren plants, skinny stalks, small tassels were characteristic of the delayed emergence. Apparently plant competition for late emerging plants has a drastic affect. 
 
Others have done similar experiments before and after these done by a young guy beginning to learn about corn.  My conclusion was that individual plants developing stalk rot were not the late emerging ones and that uniform emergence was an important factor in corn yields.  Also it was interesting that those late emergers could be confused with selfs, as confirmed by the fellow who normally evaluated hybrid purity in winter growouts.  That eventually led to developing a different purity test method.
 
My experiments were done in the 70’s with hybrids and plant densities common at that time.  It would be useful if similar experiments were done with more recent hybrids selected for consistent ear development at the higher plant densities used today.  It is notable that experiments done by others have shown that among germination test methods, the cold test is the best predictor of field emergence and that it accounts for about 70% of differences among seed lots in field emergence. 

Most corn seed planted in the USA has a seed treatment that includes at least one fungicide intended to reduce damage from Pythium.  But effectiveness is complicated by differences among Pythium species and environments.  A very recent publication in Plant Disease (http://dx.doi.org/10.1094/PDIS-04-15-0487-RE) indicated that 3 of the 4 species isolated from Iowa fields in 2014 were favored by lower temperatures (55-62°F) but one species favored a little warmer temperature of 73°F.  Although the fungicides were generally effective there were situations in which the pathogen still effectively infected the seed or seedling root.
 
It has to be complicated down there. There are the dynamics of the biology of a germinating seed, with some less vigorous than others, soils with varying water holding capacities and organic matter, and competing microorganisms.  The latter generally produce chemicals to ward off others as well.  Cell contents are leaked into the environment surrounding the seed as the seed swells and begins germination, attracting not only the zoospores of Pythium species but also numerous fungi.  The plant responds to invaders by producing phenols that can stop or slow down further invasion.  The fact that the germinating seed environment has many complicated interactions makes any attempt to give exact characterizations is difficult and contradictions to conclusions are often seen.
 
With favorable temperatures, moisture and oxygen levels, we know high quality corn seed generally overcome the potential problems with fast root and shoot growth.  We also know that every seed can be slightly different in cell membrane status because factors that includes genetics, maturity, drying, handling, and storage conditions.  Field conditions vary in soil type, temperatures and moisture levels. Pathogen intensity and seed treatment effectiveness may vary with all of the above conditions.  It is a wonder that we actually usually get 90+% stands in the fields.  It is to the credit to everyone from the corn breeder, seed producer, seed quality workers, public and private researchers and the grower that this happens.

It may seem easy to have a corn germination test.  Give the seeds water, they imbibe, and then after a few days the root and shot emerges.  Count those that do and those that do not.  However, whereas most of the seed is adequately viable, some may not be dead but have enough membrane damage that they are slow to get enough metabolism to produce undamaged seedlings at the same time as the rest of the sample.  All labs attempt to control the environmental variables such as water and temperature but interpretation of these slower plants does become a potential variable.
 
Warm tests are performed at 70-75°F.  Water is usually measured and applied automatically.  The medium may be a paper fiber similar to a disposable diaper, a rolled paper towel, sand or special artificial soil mix as we do at Professional Seed Research, Inc.  Despite attempts to be consistent between labs, and attempt to define damaged seedlings, there remains a range of results between labs when all are germinating samples from the same original bag of seed. If the average warm test germination of 30 labs is 98-100% then the range will be 95-100%. However if the average is near 90% the range will be at least 10%.  Probably this is due to small differences in lab environments and interpretation and classification of the slow and damaged seedlings.
 
Damaged membranes can repair under warm temperatures but not very well when temperatures approach the 50°F used for cold tests.  Cold test media vary between labs as they attempt to predict the emergence in the field.  In fact, the cold tests generally are a better predictor than the warm tests but also the range of results between labs is also greater.  Probably a major difference is the medium used for the tests.  Some use field soil, partly to introduce Pythium, as an attempt to mimic field conditions.  A potential problem of this medium can come from small differences in water holding capacity because this is rarely completely uniform.  This can affect the oxygen available to the seed even within a test container.  Labs do try to monitor both the medium as well as the water. The usual standard cold test is 7 days at 50°F and then 4-7 days at 70°F.  Variation between labs when testing seed from the same bag is usually greater between labs.
 
Other lab tests such as the saturated cold, advanced aging and extended cold are probably most useful in predicting the future viability of older seed. The usual problem of these tests is establishing minimum standards.  We know that seed deteriorate but the challenge is to know the slope of deterioration.
 
Ultimately a seed company needs to identify the lab method that best predicts field emergence and then make big efforts for uniformity within that lab. We are dealing with living organisms that vary in germination quality even when from the same seed field, being planted in variable field environments.  As all involved in growing corn understand, the best effort does not always match with the real world of field moistures, temperatures and soil types.

The genus Pythium is usually called a fungus although it and its relatives may not share the same origin as most fungi.  Several species of this genus have the ability to infect corn and soybeans. P. ultimum is one that is found in most fields.  Like many Pythium species, it forms thick walled spores (oospores) that remain dormant in the soil until stimulated to germinate, form a special structure (sporangium) that produces swimming spores (zoospores).  
 
The stimulant to cause germination? Leakage from germinating seed! Which seed has the most leakage, you ask?  It is those with deteriorating membranes, of course. Having cracks in the pericarp near the embryo is also associated with more leakage of metabolites from the germinating seed but most research supports the membrane damage as most significant, partly because leakage occurs through intact pericarp as well.  Pythium ultimum is favored by water logged soils and temperatures around 50°F, the same conditions that slow down the membrane repair in imbibing seed.
 
Pythium is easy to isolate from virtually any soil because of its wide host range.  It must infect roots of more plants than obvious but the plants have some resistance to stop the spread and vigorous seedlings soon outgrow the pathogen.  Drying of soil and higher spring temperatures soon favor the plant. 
 
There is one species of Pythium, P. aphanidermatum, favors higher temperatures and water soaked soils and occasionally can infect green stalks of corn causing severe lodging. It is not common for the conditions favoring this pathogen to occur in U.S.A. corn fields at midseason, and there is resistance among hybrids, reducing the occurrence of his disease.