Eyespot disease of corn

​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.