Goss Bacterial wilt of corn

​Apparent sudden 1969 appearance of this ‘new’ bacterial disease in Nebraska was a surprise.  After initial observation, it was clearly severely damaging to only a few related hybrids, especially featuring the female parent A632, a widely used component of hybrids in the northern USA corn belt.  It was also most frequent on continuous, minimum-tilled fields that had hail damage. Switching to more resistant hybrids and adjusting agronomic practices in the most affected fields, reduced the severe incidence of this disease for 30-40 years when again it appeared to be damaging in scattered fields from Indiana to Colorado. Where did it come from initially and why did it appear again several years later?
 
Surely it was occurring unnoticed, probably in both cases, before getting attention. This illustrates the difficulty of finding a new disease when the incidence is low.  The pathogen, Clavibacter michiganensis var. nebraskensis, probably originated on other grasses such as green foxtail (Setaria viridis). Perhaps it was, and is, maintained on these grasses but some mutant allowed for pathogenesis on corn. The bacterial continue to exist in corn debris that can be carried by wind to corn leaves.  With some exception, the bacteria mostly enter to the corn leaf through wounds, such as from hail and it is likely that natural infection generally occurs during heavy storms.  If the infection occurs in 3-5-leaf plants of a very susceptible genotype, the bacterial advance to completely wilt the plant.  Later infection on susceptible genotypes or on more resistant hybrids will result in elongated lesions as the bacteria tend to plug the xylem tissue.
 
Resistance can involve several genes, probably including the usual genetics for detecting the invader, communicating to adjacent cells to turn on appropriate DNA to produce anti-bacterial substances to inhibit the duplication and spread of the bacteria.  Susceptibility must involve a deficiency in this system such as the gene(s) involved in recognizing this pathogen. Such a weakness can be realized after the disease becomes frequent enough to link its damage to specific genotypes but it is difficult when occurrence is low. This probably is associated with the reoccurrence of damage to a few hybrids elsewhere in the corn belt several years later.
 
This history and genetic interaction suggest that similar problems will continue as corn hybrids, cultural practices and potential pathogens forever change.