In this issue . . .

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• Infectious Yellowing Diseases Of Watermelon In Texas
• First Report Of Puccinia sorghi Virulent On Sweet Corn With The Rp1-D Gene In Florida And Texas
• Study Shows Growers Can Control Pricing, Florida Professor Says
• Buckeye Fruit And Root Rot (syn. Phytophthora Root Rot)
• Scientists Research Using Sugars As Insecticides
• Plant-Based Vaccine Against Norwalk Virus Genetically Engineered Into Potato

Infectious Yellowing Diseases
of Watermelon in Texas

By Tom Isakeit
Associate Professor and Extension Plant Pathologist
Texas A&M University, College Station

everal different infectious yellowing diseases occur on watermelon in Texas. These diseases can be difficult to diagnose, because the symptoms can resemble pesticide toxicity or nutrient imbalances, and the pathogens themselves are difficult to isolate and study. Insect vectors are involved with many of the pathogens, further complicating diagnosis. A common feature of these diseases is that effective control measures are not available. This article is a review of yellowing diseases of watermelon that suddenly appeared in Texas over the past decade.

Why do these diseases seem to just suddenly appear? Some pathogens may be introduced through the movement of infected seed or transplants, or carried within migrating insects, but others may have been present in the growing area all along, residing in weeds and native plants. Here, these pathogens are inconsequential. But some change in the nature of an insect vector could make it much more efficient for transmitting a pathogen. So the pathogen is then moved into a crop, where it causes substantial disease. The origin of the diseases discussed in this article are not known with certainly, but an understanding of where these diseases come from could provide some insight into control measures.

Lettuce Infectious Yellow Virus (LIYV)
This is a whitefly-transmitted virus that was first detected in 1982 in the Imperial Valley of California and in Arizona. At that time, it caused serious disease not only on cucurbits, but also on lettuce. This virus has a wide host range that encompasses 15 plant families. LIYV became insignificant when the populations of the sweet-potato whitefly shifted from the A biotype to the B biotype (also known as the silverleaf whitefly, which is the predominant biotype in South Texas), because the B biotype is much less effective in transmitting LIYV. (However, the appearance of the B biotype led to the appearance of other, serious virus diseases.)

In the summer and fall of 1991, this virus was reported in Central Texas from stunted watermelon with yellow leaves, but no losses were reported. LIYV has not been detected in South Texas, where whiteflies are a persistent problem, nor has it been detected since 1991 in other parts of the state. Thus, it seems that this virus is no longer a current problem in the state.

Squash Leaf Curl Virus (SLCV)
This whitefly-transmitted virus was first identified in California in 1981. It also occurs in Arizona and Florida. It was confirmed in Texas in 1993, but it was likely present as early as the fall of 1992. Its occurrence in Texas coincided with the population explosion of the B biotype of the sweet-potato whitefly. Its distribution is South Texas, including the Lower Rio Grande Valley, and the Winter Garden areas. A whitefly-transmitted virus — probably SLCV — was identified in smellmelon from Edroy (San Patricio County), and this represents the most northern limit observed. SLCV has not been detected in far West Texas, although this is also an area where whiteflies occur. One possible explanation for this could be the lack of a native plant reservoir for the virus.

SLCV has been devastating to the production of fall-planted watermelons in South Texas, particularly in fields where seedlings are infected soon after emergence. Squash is also quite susceptible, while cantaloupes, honeydew melons, and cucumbers are not severely affected. The virus generally has a narrow host range of cucurbits, although strains in other states have wide host ranges (e.g., beans in California and cabbage in Florida).

Cucurbit Leaf-Curl Virus
This is a new whitefly-transmitted virus of cucurbits, closely related to SLCV. It appeared in 1998 in California, Arizona, Coahuila (Mexico), and the Lower Rio Grande Valley of Texas. In the Lower Rio Grande Valley, this virus is found in mixed infections with another whitefly-transmitted virus, cucurbit yellow-stunt-disorder virus. Such mixed infections can work synergistically, resulting in more severe symptoms. Mixed infections also increase the difficulty of breeding resistant cultivars for disease control.

Cucurbit Yellow-Stunt-Disorder Virus
This whitefly-transmitted virus was first identified in the United Arab Emirates in 1982, and it also occurs in Spain. It was confirmed from the Lower Rio Grande Valley in the fall of 1999, but it was probably present there a year earlier. It was also confirmed in 1999 from far West Texas (Presidio). This virus causes severe yellowing in cantaloupe, which is associated with significant yield losses, but the symptoms and impact on yield are less severe in watermelon. The virus has a host range restricted to the cucurbits.

Yellow Vine
The cause of this disease has not yet been determined, although the cause may be a phloem-inhabiting bacterium. Leafhoppers may be involved in transmission of the pathogen, since weekly insecticide applications provide some degree of control in squash. This disease was first observed in Oklahoma in 1988. It is consistently seen in the Cross Timbers Vegetational Area of Central and North Texas, although it has also been seen in East Texas. The range may be even wider, (it was documented in Tennessee in 1997). It occurs on squash, watermelon, and cantaloupe. Symptoms are generally seen 10 to 15 days before fruit maturity. Leaves turn from green to lime-yellow to bright yellow. Plants decline or wilt and collapse. There is no root rot. A key diagnostic feature is a honey-colored discoloration of phloem when the stem is cut at the crown. (Stem discoloration cause by the Fusarium wilt fungus occurs in the xylem, which is more in the center of the stem.) The severity of the disease in a region varies from year to year. Possible reasons could include differences in vector populations or movement, or differences in the abundance of pathogen hosts. There are no effective control measures, but triploid watermelons are more resistant to yellow vine than diploids.

“High Plains Yellowing” — A New Disease?
This disease was seen on isolated plants in several different fields of different cultivars in one county in the southern High Plains in 1998, 1999, and 2000. The incidence is less than 1 percent, but affected plants are noticeable from a distance because they are bright yellow, in stark contrast to surrounding green plants. There is a progressive yellowing of leaves on a vine, starting with the older leaves. Yellowing may start with the veins of a leaf, or in between the veins, but eventually, the whole leaf turns yellow. The distribution of symptomatic plants in fields suggests that an infectious disease is occurring. To date, there has been no obvious economic loss from it, though,

What Are Control Options?
There are three approaches to controlling yellowing diseases that have an insect vector:

• decreasing pathogen sources,
• decreasing vector populations, and
• decreasing plant susceptibility.

Decreasing pathogen sources may be impossible if the pathogen is widespread in weeds or native plants. This strategy could work only if an insect vector cannot migrate very far, e.g., no further than the weeds around the edge of a field. But vectors such as whiteflies can migrate several miles. In growing areas where multiple crops are possible, the use of a plant-free break between crops can prevent infection of a new crop. Destroying the fall-planted watermelons after harvest to get a plant-free period of four weeks is a key element in preventing infection of the young spring-planted crop with the squash-leaf-curl virus in South Texas.

Decreasing vector populations through the use of insecticides has generally not been successful for virus disease control. Such an approach works only if the virus increases slowly within the field during the season. However, most of the yellowing diseases are associated with initial high populations of insects, and by the time these insects are controlled, the crop is already infected.

Plant susceptibility can be decreased through cultural approaches. These include the use of transplants, since plants infected at a later stage of development are not as severely affected. Cultural approaches can work indirectly by affecting the insect vector. Row covers can effectively exclude insects, but they are not economical for watermelon production. Colored mulches, which alter insect behavior, have given mixed results in experimental trials, as have trials with stylet oils applied to foliage, which interfere with insect feeding. The use of genetic resistance in plants is very effective. Sources of resistance exist for some of the diseases mentioned here, so there is the potential to incorporate them into commercial cultivars. However, some of the viruses can genetically change over time, so plant resistance to these viruses may not be permanent.

For photographs of these diseases, see

http://plantpathology.tamu.edu/texlabn/notice.html
(scroll down and click on 'Vegetables - Watermelons').

For more information, contact Tom Isakeit by telephone at 979 - 862-1340 or e-mail at t-isakeit@tamu.edu.

Disease Notes . . .

First Report of Puccinia sorghi Virulent On Sweet Corn With The Rp1-D Gene In Florida And Texas

This report by M. C. Pate and J. K. Pataky, University of Illinois, Urbana; W. C. Houghton, Novartis Seeds, Naples, Florida; and R. H. Teyker, Del Monte Foods, Rochelle, Illinois, appeared in Plant Dis. 84:1154, 2000.

or the past 15 years, the Rp1-D gene has controlled common rust on sweet corn in North America. In August and September 1999, isolates of Puccinia sorghi were collected from Rp1-D sweet corn hybrids in Illinois, Wisconsin, Minnesota, Michigan, and New York. This was the first widespread occurrence in the continental United States of P. sorghi virulent on the Rp1-D gene [J. K. Pataky and W. F. Tracy. Plant Dis. 83:1177, 1999] Isolates of P. sorghi collected from Los Mochis, Mexico, in March 2000 had a pattern of virulence similar to the pattern for the isolates collected in the Midwest in 1999 [J. K. Pataky et al. Plant Dis. 84:810, 2000].

In April and May 2000, small uredinia were observed on Rp1-D sweet corn in Florida and Texas. In Florida, isolates were collected from six different locations within a 13-km radius near Belle Glade. Three isolates were collected each from Rp1-D and non-Rp sweet corn hybrids. Isolates also were collected from two Rp1-D sweet corn hybrids and a non-Rp sweet corn hybrid near Hondo, Texas.

Inocula of isolates were increased through one uredinial generation in the greenhouse. Several 1-cm² pieces of leaf tissue with sporulating uredinia were placed in 15 ml of a solution of water and Tween 20. This inoculum was placed in whorls of five two-leaved seedlings of a susceptible hybrid ‘Primetime’. Urediniospores from newly formed uredinia were collected 10 days later and used as inocula to assay each isolate. Two isolates from Florida (one each from an Rp1-D and a non-Rp hybrid) were assayed on the non-Rp susceptible check, 20 different single Rp genes, and nine compound Rp genes. Other isolates were assayed on two replicates of a non-Rp susceptible check, a source of Rp1-D, and five single Rp genes that were effective against the isolates collected from the Midwest in 1999 and from Mexico in 2000.

Each experimental unit consisted of five plants grown in 10-cm-diameter pots. Plants at the two-leaf stage were inoculated three times within 5 days by filling whorls with a urediniospore suspension. Rust reactions were rated 10 days after the final inoculation.

Isolates collected in Florida from non-Rp hybrids were avirulent on Rp1-D, but those collected in Texas from non-Rp hybrids were virulent on Rp1-D. Isolates collected in Florida and Texas from Rp1-D hybrids had a similar pattern of virulence as isolates collected from the Midwest in 1999 and from Mexico in March 2000; that is, effective single Rp genes included Rp1-E, Rp-G, Rp1-I, and Rp1-K. A source that we previously believed was Rp1-L now appears to be Rp-G.

These are the first reports from Florida and Texas of P. sorghi virulent on Rp1-D, and they are the first occurrences of virulence against Rp1-D in the continental U.S. in 2000. Apparently, P. sorghi with virulence against Rp1-D has become established in an area where common rust inocula for North America overwinters.

Study Shows Growers Can Control Pricing,
Florida Professor Says

This article by Tracy Rosselle, Eastern Editor,
appeared in The Packer, September 11,2000.

NAPLES, Fla. — A scientific study meets the real world.

That’s one way to characterize John VanSickle’s presentation at the Florida Tomato Institute proceedings September 6 in Naples. VanSickle, a professor in the University of Florida’s food and resource economics department, told Florida producers they should re-evaluate some of their commonly held perceptions about who controls the pricing point of fresh tomatoes in the vertical marketplace.

“You control more of your destiny today,” VanSickle told an audience of mostly skeptical tomato producers. “You have a stronger position today than you had 20 years ago.”

In an age of buyer consolidation and often horrendous returns to growers, those words seemed to come from left field. Figures recently released by the U. S. Department of Agriculture’s Economic Research Service, in fact, show sales of Florida tomatoes plummeted 24 percent in 1999. But VanSickle presented findings that contradict the widely held belief of many in the Florida tomato deal, that retailers are exerting power over producers. The findings also suggest previous studies on the derivation of prices are outdated.

VanSickle said econometric data gathered by researchers in his department show pricing relationships between the producer and retail sectors are symmetric. For example, price increases and price decreases at the producer level are passed on to consumers in equal measure at retail. What’s more, as the produce industry has moved toward direct marketing — more often bypassing brokers and terminal market operators — producers may have been granted more leadership in the pricing function. Instead of wholesale markets dictating prices to both producers and retailers, as previous research showed, producers now appear able to set prices more efficiently.

Florida’s tomato producers historically have been price takers, and now don’t fully appreciate the pricing opportunities they have, VanSickle said following the presentation. A more cooperative approach to marketing tomatoes from the supply side could boost returns dramatically, he said.

There’s even talk of revising existing anti-trust laws to bring the provisions of the Capper-Volstead Act, which allows competing domestic producers to discuss prices under certain circumstances, into the international marketplace, he said. That potentially would mean Florida tomato producers cooperatively discussing marketing plans with producers in Mexico, the Netherlands, Canada, and elsewhere.

For now, though, suggesting that tomato producers are the ones with market leverage remains a hard sell. Preliminary findings from the on-going ERS study on retail consolidation appear to show Florida tomato shippers are, in fact, shipping less product direct to retailers than in past year. Bob Spencer, sales manager for Palmetto-based West Coast Tomato Inc., said the proliferation of tomato varieties means Florida’s field-grown product is getting less retail shelf space than in years past — hardly the stuff of price-setting leverage.

Buckeye Fruit and Root Rot
(syn. Phytophthora Root Rot)

This article appeared in the ‘Disease Identification’ section
of The Tomato Magazine.

Causal Agent: phytophthora parasitica, P. capsici, P. dreshsleri

Distribution: Worldwide

Symptoms: These fungi can infect all parts of the plant. They can cause a damping-off of seedlings, a root and crown rot, a foliar blight and a fruit rot. The symptoms caused by root rot are water-soaked brown lesions on the secondary roots and the taproot that can extend above the soil-line into the stem. As the disease progresses, the smaller roots collapse and decay, and large brown, sunken lesions develop on the larger secondary roots and the tap root. A longitudinal section through the taproot reveals a chocolate-brown discoloration of the vascular system that extends a short distance beyond the lesion. Severely infected plants eventually wilt and die. Infected leaves initially develop water-soaked, irregular-shaped lesions that quickly collapse and dry. Stem lesions can develop at any level on the stem, but are typically found near the soil-line. The lesions are first dark green and water-soaked, and eventually turn dry and brown. As the lesions expand, they can completely girdle the stem, with the pith becoming brown and collapsing. The fruit symptoms start as grayish-brown, water-soaked lesions that can expand, rapidly forming brown, concentric rings that resemble a buckeye nut, hence the name. The brown discoloration can extend into the fruit center, with the young green fruit becoming mummified, while the mature fruit quickly rots from invasion by secondary organisms.

Conditions for Disease Development: These fungi have a relatively wide host range, and can survive in the soil and infested plant debris for at least 2 years. They can be spread through irrigation run-off and on farm equipment. Initial infection is favored by moderate soil moisture levels and moderate temperatures (20 degrees C, 68 degrees F.). Excessive irrigation or rain, in combination with heavy or compacted soils, favor further disease development.

Control: Fungicides can help reduce losses from this disease. In addition, cultural practices that can help reduce losses include using a 3-year rotation to non-host crops, improving soil drainage, avoiding soil compaction, using raised beds to improve drainage, and using shorter irrigation times to avoid extended periods of soil saturation.

Scientists Research Using Sugars As Insecticides

This article appeared in The Grower, September 2000.

ugar esters tested by Agriculture Research Service and university entomologists around the country could find use as environmentally friendly insecticides. The esters are lethal — almost immediately — to nearly all mites and soft-bodied insects, such as whiteflies, aphids, thrips, and pear psylla that they contact. Then they degrade into harmless sugars and fatty acids.

These sugar esters do little harm to beneficial predatory insects, and are non-toxic to animals and humans. Some are even approved as food-grade safe. And because of how the esters work, insect pests are not expected to develop resistance to them anytime soon.

The control concept originated about a decade ago. Now, four years of testing have shown the sugar esters to be as good as — or better than — conventional insecticides against mites and aphids on apples; psylla on pears; whiteflies, thrips, and mites on vegetables; and whiteflies on cotton.

Like insecticidal soaps, the esters kill insects by either dissolving their protective waxy coatings or suffocating.

ARS and AVA Chemical Ventures of Portsmouth, New Hampshire, have applied for a patent. The company hopes to market the first of these sugar ester compounds by the end of this year, pending U. S. Environmental Protection Agency registration.

Plant-Based Vaccine Against Norwalk Virus
Genetically Engineered Into Potato

This article appeared in The Vegetable Growers News, September 2000.

uman immunity to a virus has been triggered for the first time by a vaccine genetically engineered into a potato. The specific virus involved is the pervasive Norwalk virus — the leading cause of food-borne illness in the United States and much of the developed world.

Scientists from the Boyce Thompson Institute (BTI) for Plant Research at Cornell University and the University of Maryland School of Medicine at Baltimore report on the success of the first human clinical trials of the plant—based vaccine in the July 2000 issue of the Journal of Infectious Diseases.

“This plant-based vaccine could be the first one readily accepted in the developed world. It’s very exciting,” says Charles Arntzen, president and chief executive of BTI. “It’s likely that in the United States, this Norwalk virus vaccine could easily be the first licensed product based on our plant biology research.” Arntzen and his colleagues previously conducted a successful clinical trial in triggering immune response in humans to the bacterium Escherichia coli through a transgenic potato vaccine. The results were published in Nature Medicine in 1998.

The first of three stages of human clinical trials for the Norwalk virus plant-based vaccine began in April 1999, and was conducted at the Center for Vaccine Development at the University of Maryland. Volunteers ate two or three doses of BTI-developed transgenic, raw potato containing the viral antigen. Overall, 19 of the 20 volunteers (95 percent) who ate the transgenic potatoes developed an immune response to the Norwalk virus. Before eating the potatoes, the volunteers were tested for Norwalk antibodies, and all indicated previous exposure to the virus.

The Center for Disease Control and Prevention in Atlanta estimates that more than 23 million people in the United States are infected annually by the Norwalk virus, or by Norwalk-like viruses. That compares to 79,000 cases resulting from E. coli contamination, 2,500 cases of listeriosis, and 1.4 million cases of illness from salmonella.

Norwalk virus received its name in 1968 when nearly 100 students in a Norwalk, Ohio, school simultaneously came down with nausea, vomiting, stomach cramps, and diarrhea. It was not until four years later that scientists realized the pathogen was a virus. Until 1990, scientists and doctors routinely blamed common food-borne disease symptoms on bacterial pathogens. Microbiologist Mary Estes and others at the Baylor College of Medicine in Houston cracked the Norwalk virus’ genetic code 10 years ago, and scientists routinely began testing for it.

The BTI/University of Maryland report, “Human Immune Responses to a Novel Norwalk Virus Vaccine Delivered in Transgenic Potatoes,” was authored by Arntzen; Estes; Hugh Mason, a senior scientist at BTI; and by Genevieve Losonsky, Carol Tacket, and Myron Levine of the University of Maryland School of Medicine. The research was funded in part by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health.

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