Establishment of new corn diseases

​Ht1 gene for resistance to Exserohilum turcicum, cause of northern corn leaf blight, was incorporated in most US hybrids during the 1970’s.  This gene was responsible for reacting to initial infection by this fungus by producing a toxin to the fungus in the area of infection that prevented the fungus from producing spores to spread the disease to other plants within the field.  In 1979, it was reported that a seed field of corn with that gene had been attacked by E. turcicum producing lesions with spores.  Inspection of fields in many locations in the USA discovered the same phenomenon.  A gene in the fungus, apparently not previously frequent among the genome, was greatly favored over those variants of the fungus with limited production due to the Ht1 gene in corn, had built up an intensity until it was noticed by the right humans to identify the new race. 
 
This type of genetic battle between host species and potential pathogens is continual.  Most potential pathogens are controlled effectively by resistance mechanisms in corn either intentionally by corn breeders screening for resistance when the crop is intentionally exposed to the pathogen.  Most damage occurs when new environments favor a variant of the pathogen that allows it to overcome host resistance systems.  It is probable that the pathogen variant occurred for several seasons only to gradually build up intensity to be noticed and identified.
 
Corn Lethal Necrosis, also known as Maize Lethal Necrosis, develops into a damaging corn disease when Maize Chlorotic Mottle Virus (MCMV) and another virus infect the same plant.  Both viruses have separate insect vectors.  Although MCMV had not been found in the USA until the outbreak of damage from the disease, it was later found that this virus was found in multiple locations, but absence of other viruses prevented notable disease development.
 
Race T of Bipolaris maydis, cause of the epidemic of southern corn leaf blight had a gene that attacked the mitochondria associated with male sterility of corn.  The bacterium causing Goss wilt probably is a mutant of a common grass pathogen.  Pathotype 4 of Bipolaris carbonum, cause of very minor pathogen of corn, had a gene that specialized in attacking a common inbred used in many corn hybrids.  
 
There are multiple examples in the many places that corn is grown where the genetics of the pathogens, the corn and environments result in development of what appear to be new diseases.  In all cases, efforts by corn specialists identify these factors and reduce the damage by selection of resistance and/or changing the environment that favors the pathogen.

​There is no reason to believe that this will not continue.  We benefit from the broad genetics in Zea mays.