| Stewart's Wilt | |
|---|---|
| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Proteobacteria |
| Class: | Gamma Proteobacteria |
| Order: | Enterobacteriales |
| Family: | Enterobacteriaceae |
| Genus: | Pantoea |
| Binomial name | |
| Pantoea stewartii (Smith 1898) Mergaert et al. 1993 |
|
| Subspecies | |
|
P. s. subsp. stewartii |
|
| Synonyms | |
|
Pseudomonas stewarti (sic) Smith 1898 |
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Stewart's Wilt is a serious bacterial disease of corn caused by the bacterium Pantoea stewartii. This bacterium affects plants, particularly types of maize or corn such as sweet, flint, dent, flower and popcorn.[1] The disease is also known as bacterial wilt or bacterial leaf blight and has shown to be quite problematic in sweet corn in the gram negative state of bacterium.[2][3] The primary vector of Pantoea stewartii is the corn flea beetle, (Chaetocnema pulicaria).[4] The bacterium overwinters in the gut of the adult beetle during the winter and come spring, is spread when adult beetles feed on the plant seedlings.[1] The bacteria have also been known to spread from the endosperm of the plant seed to the young seedlings, but this is quite rare and its incidence is insignificant compared to insect transmission.[4] Thus, survival of the insect vector through the winter months, especially in the north central U.S., is the key factor in development of the disease. The disease manifests in two phases: seedling wilt, when the growing point dies; and leaf blight, white lesions on the leaves of older plants. Sweet corn has proven to be more susceptible than field corn, although some hybrids and inbreeds of popcorn and field corn are highly susceptible. One of the first forecasting systems designed was for preventing Stewart's Wilt.[5] Apart from forecasting, Stewart's wilt severity can be controlled effectively through use of insecticides and resistant hybrids of corn, with resistant hybrids being the best means of control.[6]
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Stewart's wilt can be a serious disease of many corn types, including: sweet, dent, flint, flower, and popcorn.[1] Sweet corn and popcorn cultivars are more susceptible to Stewart's wilt than field (dent) corn, but there are some dent corn inbreds and hybrids that are susceptible. Stewart's wilt causes yield reductions by decreasing the size of corn stand or by limiting the production of corn. This results in fewer and smaller ears of corn.[6] In the United States, the eastern parts of the corn belt have been known to have problems with Stewart's wilt. Other parts of the country may only encounter occasional damage from this disease. Damage to sweet corn usually occurs at the seedling stage where the seedlings wilt and die.[1]
Stewart’s wilt has two phases of symptoms: the wilt phase and the leaf blight phase. For both phases, symptoms first appear as leaf lesions, initiating from corn flea beetle feeding scars. At first, the leaf lesions appear long and irregularly shaped and are light green to yellow and later on, straw colored. On mature plants, yellowish streaks with wavy margins extend along the leaf veins.[2] This leaf blight phase is often prevalent after tasseling and the symptoms look similar to frost damage, drought, nutrient disorders, northern corn leaf blight (caused by Exserohilum turcicum), and particularly Goss's wilt (caused by Clavibacter michiganensis ssp. nebraskensis).[6] A good way to determine if the corn is facing symptoms from Stewart's wilt, is to look at the leaf tissue under microscope. If the bacterial ooze exhibits nonflagellate, nonspore-forming, rod-shaped bacterium, there's an great chance it's Stewart's wilt.[5]
The corn flea beetle feeds on corn leaf tissue and then transmits the bacteria, Pantoea stewartii, into the plant. When large populations of corn flea beetles are feeding, skeletonization of leaves and death of seedlings can occur.[7]
In most cases, the wilt phase occurs on seedlings, but for certain corn types (i.e. sweet corn) more mature plants can become wilted. The wilt phase is systemic, meaning the majority of the plant is infected via bacterial movement and colonization of the plant's vascular system. When the bacterium spreads within the plant, leaves begin withering and can die. Plants become stunted and at times, the whole plant may wilt and die. Dwarfed, bleached tassels are common. Often, plants that have wilt symptoms will also have leaf blight symptoms.
When the bacteria reach the corn stalks, the vascular bundles become brown and necrotic. A good indicator of whether or not the bacteria has infected the stalks is if there are yellow masses of bacteria oozing from the vascular bundles. With certain sweet corn hybrids, yellow, slimy ooze collect on the inner ear husks and/or cover the corn kernels. It's possible that the kernels may also have grayish lesions with dark margins or they may be irregular in shape and dwarfed. Another common symptom of the bacteria is formation of open cavities within the stalk tissue. While the plants are weak and vulnerable, stalk rot fungi can further invade the corn plant.[8]
Chaetocnema pulicaria, the primary vector for Pantoea stewartii, overwinter as adults and will begin feeding on corn seedlings early in the spring season. The bacterium overwinters in the gut of the adult corn flea beetles. Warmer winter temperatures will allow for greater beetle survival and in effect, higher populations come spring. Emerging beetles in the spring transmit the bacteria into corn leaf tissue through feeding. The corn flea beetles wound the leaf and contaminate the wounds with insect frass (excrement), which additionally contains the bacteria. Once the bacteria are inside the plant, they multiply and fill the xylem and intercellular spaces of the leaf. The degree of multiplication is highly dependent on susceptibility of the cultivar. Highly susceptible plants become systemically infected and face symptoms such as stunting, wilting, and even death. In less severe cases, a plant may show leaf lesions that are long and irregularly shaped. Some genotypes are able to greatly restrict pathogenic growth. In such plants, the leaf lesions are short, insignificant may even be non-existent. In certain corn varieties, kernels can be infected later in the growing season after flowering occurs. Although corn kernels can be a source of inoculum, seed transmission is quite rare.[8]
The number of flea beetles emerging in spring from hibernation depends on the severity of winter temperatures. Warm winter temperatures favor the survival of flea beetle vectors and increase the risk of Stewart’s disease. Low temperatures are highly unfavorable for beetle survival. The numbers of emerging adults can be estimated by calculating a winter temperature index by averaging the mean temperatures (expressed in °F) for December, January, and February. If the sum of the mean temperatures is 90°F or greater, the beetles will survive in high numbers and the disease risk is high; if the sum is between 85° and 90°, the risk is moderate to high; 80° to 85°, moderate to low; and a sum less than 80°F represents low risk.[8]
Flea beetles do not survive in the northern half of Illinois due to low winter temperatures. Those found in late spring or summer have migrated from the south. Snow or other winter cover apparently has little effect in providing sufficient shelter to enhance survival of the overwintering flea beetles. Prolonged periods of wet summer weather are unfavorable for beetle multiplication and feeding, while dry weather is favorable. Consequently, although this disease has been found throughout the world, the bacterium has never survived and spread other than in North America. The reason for this is because the disease depends on where Chaetocnema pulicaria occur. In North America, Stewart’s wilt is found in the mid-Atlantic and the Ohio River Valley regions and in the southern portion of the Corn Belt. This region includes parts of Connecticut, Delaware, Illinois, Indiana, Iowa, Kentucky, Maryland, Missouri, New Jersey, New York, Ohio, Pennsylvania, Rhode Island, Virginia, and West Virginia. Stewart’s wilt can also be found in eastern and midwestern states and prtions of Canada, but this depends on whether or not the corn flea beetles survive the winters. Corn flea beetles can transmit the bacteria northward during the summer, but if the insect vectors cannot survive the harsh winter temperatures, then the bacteria cannot be spread.[9] The toothed flea beetle, adult 12-spotted cucumber beetle, seed corn maggot, wheat wireworm, white grubs, and larvae of corn rootworms can also carry Pantoea stewartii from one plant to another during the summer. These pests cannot overwinter and transmit this disease.[4]
Forecasting should be done to determine the severity of Stewart's bacterial leaf blight. Prediction relies on temperatures from previous winters. A way to determine if an outbreak of Stewart's wilt will occur is to add the average temperatures in December, January, and February. If you find them to be greater than 95 degrees Fahrenheit, expect an outbreak. If you get a sum of the average temperatures to be less than 90 degrees Fahrenheit, there's usually no need for control. This forecasting method solely relies on the corn flea beetle's ability to overwinter. As you'd imagine, a winter with numerous days below 0 degrees Fahrenheit will reduce beetle populations and lessen the risk for disease. On the other hand, high amounts of snow cover and heavy crop residues are thought to favor beetle survival; even when temperatures are lower than 0 degrees Fahrenheit. When forecasting for this disease, snow cover and temperatures must be analyzed before assessing control of the disease.[1]
All sweet corn varieties are susceptible to wilt in the first leaf stage. Susceptibility decreases and natural control is obtained as plants grows older. External disease control is conducted by insecticide spraying to stop early feeding of overwintering flea beetles.[1] Insecticides should be sprayed as soon as corn first breaks the soil surface. When establishing control measures, spraying should be repeated several times to regulate the presence of the insecticide products in the field.[10] Common insecticides used for control of Stewart's wilt are clothianidin, imidacloprid and thiamethoxam. These insecticides are most effectively used at rates of 1.25 (mg ai/kernel), with clothianidin being the most effective at that rate. Application rates on the labels may vary a little, so follow the label rates for each insecticide.[11] Better results are obtained when seeds are sprayed prior to germination. In furrow spraying and post-germination foliar spraying may not be effective.[5]
Although insecticides are effective, resistant hybrids are the best means of disease control. There's less chance of resistance and they've all together showed better results for protection against Stewart's disease.[6] Hybrid varieties of sweet corn are also available for control. Dent corn hybrids are more resistant to the disease than sweet corn and hence, do not require insecticides.
In sweet corn, losses are as significant as hybrid varieties, but are only utilized on a periodic basis. The susceptible varieties cause losses ranging from 40-100% when infected prior to the 5-leaf stage. The losses are 15-35% and 3-15% for 7-leaf and 9-leaf stage respectively. Stewart's wilt may add additional costs for phytosanitary regulations from trading partners. Such regulations primarily affect seed commerce by preventing seed from being exported or by creating additional costs for phytosanitary inspections prior to export. During epidemics in the 1990s, Stewart's wilt was a significant economic issue for the corn seed industry because of the logistics of trading and exchange of large volumes of field corn seed throughout the world. Stewart's wilt also creates indirect costs for seed producers because resources must be used to screen germplasm and breed corn for Stewart's wilt resistance in order to develop hybrids that efficiently and effectively control the disease.[5] In Kentucky, the disease causes huge losses for corn producers. Stewart's wilt impacts include stand reductions, production of fewer and smaller ears, and an increased susceptibility of wilt-infected plants to stalk rotting organisms.
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.[5]