Origin
Stewart's wilt was first observed by T.J. Burrill in the late 1880s while studying fire blights in the corn fields of Southern Illinois. Mr. Burrill associated the symptoms he found with dry weather and chinch bug damage, yet he indicated that bacteria could be the cause for the disease. Nonetheless, he was unable to complete Koch's postulates to determine the causal pathogen of the disease.
Then, in 1895, F.C. Stewart observed wilt in sweet corn plants in Long Island, NY. After completion of Koch's postulates with the bacteria in sweet corn, Stewart gave an accurate account of the symptoms and named the pathogen Pseudomonas stewartii in 1898. With the help of his colleagues, Stewart concluded that the bacteria was readily disseminated by seed. Another 25 years later, in 1923, a corn flea beetle, Chaetocnema pulicaria, was identified as the primary vector responsible for the mid-season spread of the disease.
The taxonomy of the pathogen was under debate for half a century, when in 1963, D.W. Dye named it Erwinia stewartii. Dye did so because the pathogen is closely related to other bacteria in the Erwinia herbicola-Enterobacter agglomerans complex. Recently, the complex was assigned to the genus, Pantoea, which did not agree with the results from the 16S RNA sequence analysis. Due to this difference, the pathogen was named, Erwinia stewartii, and has most recently been named, Pantoea stewartii.
Stewart's wilt was primarily responsible for the development of the first widely grown, single-cross hybrid, 'Golden Cross Bantam'. In 1923, Glenn Smith, a USDA scientist working at Purdue University, created a hybrid from two different lines of the regular, susceptible 'Golden Bantam'. The hybrid was tested in one of the most destructive epidemics of Stewart's Wilt in Northern Indiana. After a successful performance, the hybrid was legalized and named Golden Cross Bantam. Within a few years, 70-80% of the sweet corn canned in the US was Golden Cross Bantam. Due to its history, Erwinia stewartii is a model organism for genetics of pathogenicity and quorum-sensing regulation of gene expression.
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