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Egusi seed photographWatermelon Crop Information

Disease, Insect, and Stress Resistance

  • by Todd C. Wehner
  • Department of Horticultural Science
  • North Carolina State University
  • Raleigh, NC 27695-7609

Disease

Seedling Tests. Disease resistance is an important objective of most breeding programs. Screening for resistance to several important diseases using greenhouse seedling tests is useful, and provides several advantages. Plants that are found to be resistant to the diseases being tested can be transplanted from the test flats to soil or other growth medium in bags or pots where they can be grown and self-pollinated, or crossed with other lines. Greenhouse tests can be run at a time when plants cannot be grown outside, permitting more generations of testing each year, and the disease testing greenhouses can be isolated from other watermelon research to keep the diseases from spreading. At North Carolina State University, gummy stem blight tests are isolated in one area, and virus tests in another area so that the diseases do not spread to a third area where the other breeding work is located.

For some diseases such as anthracnose, it is useful to have a humidity chamber to incubate the disease after inoculation. A humidity chamber can be built on a greenhouse bench using one humidifier for each 24 sq. ft. of bench area. An air conditioner can be used to keep the temperature cool, since some diseases do best in cool and humid conditions. The greenhouse temperature is usually kept between 75° and 95°F for optimum plant growth, and the humidity chamber is usually kept between 65° and 75°F for optimum disease development. A less expensive option for disease chambers is to build a frame on a greenhouse bench and cover it with polyethylene film on the top and sides. Humidifiers placed inside the chamber several hours before disease inoculation should be able to raise the relative humidity above 95%.

Fusarium Wilt. Fusarium wilt is caused by Fusarium oxysporum f. sp. niveum (see Figs. 7.17-7.20). The disease was first reported in 1889 in Mississippi, and was widespread throughout the southern parts of the United States by 1900. Three types of pathogen spores are commonly observed: small, colorless, oval, non septate microconidia; large, sickle shaped, septate macroconidia; and thick walled circular chlamydospores. There are three races known: 0, 1, and 2. Most current varieties are resistant to race 0, and some also are resistant to race 1. Race 2 was discovered more recently, and occurs mainly in the south central production areas such as Texas and Oklahoma, but it also has been found in Florida.

Race 0 causes wilt in older, susceptible varieties such as ‘Florida Giant’, ‘Black Diamond’, and ‘Sugar Baby’. Race 1 is more virulent than race 0 and affects more plants within susceptible varieties, but does not affect resistant 'Calhoun Gray'. Race 2 is highly virulent and can affect otherwise resistant varieties such as 'Calhoun Gray', 'Summit', 'Smokylee', and 'Charleston Gray'. Races of fusarium can be identified using differentials. 'Sugar Baby' and 'Black Diamond' are susceptible to all the three races; 'Quetzali', 'Mickylee', 'Charleston Gray', and ‘Crimson Sweet’ are susceptible to races 1 and 2, while 'Calhoun Gray' is susceptible to only race 2. Resistance to race 2 is available in PI 296341 and PI 271769.

  • Fusarium wilt race
  • 0 1 2 Variety or accession
  • S S S Black Diamond (or Sugar Baby)
  • R S S Quetzali (or Mickylee)
  • R M S Charleston Gray (or Crimson Sweet)
  • R R S Calhoun Gray
  • R R R PI 296341 (or PI 271769)

Fusarium can survive in soil as a saprophyte. The pathogen is spread locally by moving soil, compost, manure, water, tools, and machinery from one field to another, as well as by humans and animals moving between fields. The pathogen can also persist on infested seeds for more than 2 years.
Fusarium enters plants through root tips and openings in roots where lateral roots emerge. Presence of root-knot nematodes is also thought to increase the incidence of the disease. After penetration, the fungus grows into the xylem where it accumulates materials that plug the xylem and cause wilting. Watermelon is attacked at all growth stages by the pathogen. At the seedling stage there is damping-off, and cotyledon wilt results in slower growth and stunting. The vascular tissue inside wilted stems may be discolored. A white or pink colored fungus growth usually appears on the surface of dead stems in wet weather conditions. The ideal temperature for infection and disease development is 80°F. However, seedling rot occurs at soil temperatures of 61 to 65°F, while seedling wilt is severe between 77 to 82°F. The disease is also promoted by high soil organic matter.

The first fusarium wilt resistant variety ‘Conqueror’ was released in 1908. It was developed by W.A. Orton of the USDA using a wilt-resistant citron accession crossed with 'Eden'. 'Conqueror' did not have high fruit quality, so was not grown much after its release. However, varieties developed using resistance from 'Conqueror' such as 'Iowa Belle' and 'Iowa King' had improved fruit quality, so were used commercially. More recent varieties such as ‘Calhoun Gray’, ‘Smokylee’, and ‘Dixielee’ have resistance, as well as improved horticultural performance.

Two types of fusarium wilt resistance are known, having different patterns of inheritance. Resistance to race 1 in 'Calhoun Gray' is controlled by a single dominant gene, with some modifier genes, and provides a high level of resistance that is easy to transfer into new breeding lines. There is also a source of resistance to race 1 which is controlled by several recessive genes. That source of resistance has been difficult to fix at a high level in stable, inbred lines. Varieties resistant at high inoculum levels are 'Dixielee' and 'Smokylee'. In wild species, resistance to fusarium has been reported to be polygenic. Resistance to race 2 has been reported in PI 296341, and the selection PI 296341-FR is resistant to all three races of fusarium. Also, PI 271769 was reported to be highly resistant to race 2.

Anthracnose. Anthracnose caused by Colletotrichum lagenarium is an important disease of watermelon in the United States (see Figs. 7.3-7.6). Symptoms caused by this pathogen may occur on leaves, stems, and fruit. Lesions on leaves are irregular shaped, limited by the leaf vein, and brown to black in color. Lesions on the stem are oval shaped and tan colored with a brown margin. Lesions similar to those found on stems and leaves also appear on the fruit. Older fruit show small water-soaked lesions with greasy, yellowish centers that are somewhat elevated.

Seven races of the anthracnose pathogen have been reported. Races 4, 5, and 6 are virulent in watermelon, but races 1 and 3 are most important. Many varieties are resistant to races 1 and 3, and resistance to race 2 will be needed in the near future.

The first source of resistance to anthracnose was identified in an accession, Africa 8, sent to D.V. Layton of the USDA by R.F. Wagner in Umtali, South Africa. Layton developed anthracnose resistant 'Congo', 'Fairfax', and 'Charleston Gray' from that source. Resistance was later found to be inherited as a single dominant gene, Ar-1. The gene provides resistance to races 1 and 3, but not to race 2. 'Crimson Sweet' and many other current varieties have that source of resistance. Several genes were found to be responsible for resistance to Race 2.

PI 189225, PI 271775, PI 299379, and PI 271778 have been reported to carry resistance to complex Colletotrichum species. Some of the other sources of resistance to anthracnose reported in the literature are PI 203551, PI 270550, PI 326515, PI 271775, PI 271779, and PI 203551. 'R 143' was reported to be resistant to race 2 of the pathogen. PI 512385 had the highest resistance to race 2 of the pathogen from a screening test involving 76 plant introductions.

Gummy Stem Blight. Watermelon is one of the most susceptible of the cucurbit species to gummy stem blight, caused by Didymella bryoniae (see Figs. 7.21-7.25). The disease occurs throughout the southern United States, particularly the southeast. Field and greenhouse tests are available, but the results are variable, and it can be difficult to get reproducible results.

The USDA collection of plant introduction accessions has been screened for gummy stem blight resistance by several teams of researchers. Some accessions have resistance to the disease, including PI 189225 and PI 271778.

Powdery Mildew. Watermelon is one of the most resistant cucurbit species to powdery mildew (Sphaerotheca fuliginea) (see Figs. 7.28-7.30). However, there are a few regions of the world where powdery mildew is a problem on watermelon. For example, watermelons grown in southern India are affected with the disease, but not in northern India. In southern India, 'Arka Manik' is resistant to powdery mildew. The pm gene causes susceptibility to the disease, but most varieties have the resistance allele. Powdery mildew is becoming more of a problem in the United States, especially in the western states, and has been reported in the southeastern states as well.

Yellow Vine. Yellow vine is a relatively new disease of watermelon, caused by an unknown, phloem-limited bacterium. Evidence indicates that leafhoppers vector the disease. The disease was first observed in central Texas and Oklahoma in 1991 and has caused severe losses in early-planted watermelon in some years. In 1998, the disease was detected in watermelon and pumpkin in Tennessee. Production areas of Georgia, Florida, and other parts of southeastern United States may be at risk in the future. Low levels of resistance or tolerance have been identified in a few open-pollinated and hybrid varieties, although the mechanism of resistance is unknown. Research is needed to identify good sources of resistance.

Bacterial Fruit Blotch. Bacterial fruit blotch of watermelon is a serious disease of seedlings and fruit caused by Acidovorax avenae subsp. citrulli (see Figs. 7.8-7.13). Disease incidence increases under high humidity or where overhead irrigation is used. The disease was first reported to occur in commercial watermelon production areas in the United States in 1989. Early-season outbreaks can result in total loss of fruit by harvest time. Bacterial fruit blotch is also reported to attack cantaloupe fruit in the field, as well as other cucurbits. Bacterial fruit blotch epidemics during 1994 in certain states in the United States resulted in litigation, and had a devastating effect on the watermelon industry. Currently, most seed companies require growers to sign waiver forms to reduce the possibility of litigation. Some companies have restricted seed sales in certain states where the risk of disease is high. Seed costs have increased due to the changes in the seed handling, packaging and testing required for reducing the incidence of disease.

The characteristic symptoms of bacterial fruit blotch are the appearance of a dark olive green stain, or blotch, on the upper surface of infected fruit. Apart from attacking the fruit, the pathogen is also reported to attack the leaves and seedlings, and can be seed transmitted. D.L. Hopkins and co-workers reported that fermentation of seeds for 24 to 48 hours followed by 1% hydrochloric acid or 1% calcium hypochlorite treatment for 15 minutes prior to washing and drying were the most effective treatments for bacterial contaminated watermelon seeds. This treatment is for diploids; triploid seed germination is drastically reduced by fermentation. However, an effective, cost efficient, and environmentally safe method for disease control would be development of resistant varieties.

A seedling test for early screening of watermelon fruit blotch was developed in 1992, and research on a few watermelon lines using this test has been reported. There has been some research to identify genetic resistance in the watermelon germplasm collection. Based on seedling tests, PI 295843 and PI 299378 were reported to be resistant to the pathogen. In 1993, D.L. Hopkins and co-workers conducted a study of 22 varieties and 2 PI accessions for resistance to fruit blotch of watermelon and reported that none were immune to the pathogen. Research is underway to find sources of resistance in the germplasm collection.

Fruit resistance to the pathogen appears to be related to rind color and ploidy, with diploid varieties having light rind color being most susceptible and triploid varieties with dark rind color being less susceptible. Fruit with stripes appeared to be intermediate in their resistance. Detached leaf tests have been developed that are effective in screening plants for resistance in a breeding program.
Bacterial Rind Necrosis. Bacterial rind necrosis is caused by Erwinia species. However, some other bacterial species (Pseudomonas, Enterobacter, and Bacillus) are also known to cause similar symptoms. Typical symptoms of bacterial rind necrosis on watermelon fruit are characterized by a light brown, dry, hard area of discoloration interspersed with light areas generally limited to the rind (see Fig 7.7). The disease was first reported in Texas in 1968. The most resistant varieties in studies conducted in Florida over a 3-year period were 'Sweet Princess' and 'Jubilee', while the most susceptible were 'Klondike Blue Ribbon' and 'Louisiana Queen'.

Root-knot Nematodes. Watermelon is susceptible to root-knot nematodes caused by Meloidogyne spp. (see Figs. 6.1-6.3). The USDA collection of plant introduction accessions is being screened for resistance. Root-knot resistance may be an important future breeding objective if resistant accessions are identified.

Virus Diseases. The main virus problems in watermelon production in the United States are papaya ringspot virus-watermelon strain (PRSV-W, formerly watermelon mosaic virus-1), watermelon mosaic virus-2 (WMV-2) (see Figs. 7.32-7.33), and zucchini yellow mosaic virus (ZYMV). The watermelon germplasm collection has been screened for resistance to some virus diseases. Accessions reported to be resistant to WMV-2 are PI 244018 and PI 244019. Resistance to ZYMV is found in PI 482299, PI 482261, PI 595203, and PI 255137. Research is in progress to identify sources of resistance to PRSV-W as well. Multiple virus resistance will be an important breeding objective for new cultivars in a few years.

Other Diseases. Verticillium wilt is an increasing problem in the western United States, but little is known about sources of resistance. Resistance to alternaria leaf spot (see Figs. 7.1-7.2) has been identified in varieties such as ‘Sugar Baby’, ‘Fairfax’, and ‘Calhoun Gray’.

Physiological Diseases. Many of the watermelon fruit defects have a genetic component. Breeders should select lines to be free of defects under conditions conducive to the problem. Fruit defects include hollowheart (see Fig. 7.34), rind necrosis (see Fig. 7.7), blossom-end rot (see Fig. 7.35), and cross stitch (see Fig. 7.38). Hollowheart is a separation of the tissue within the endocarp caused by rapid fruit growth and weak tissue. More research is needed to identify sources of defect resistance, and environmental conditions that help reduce their frequency.

Insect Resistance Traits

Little research has been done on insect resistance in watermelon. This may be due to the fact that most insect pests can be controlled with insecticides. The major insect and arachnid (arthropod) pests of watermelon are aphids (see Figs. 8.1-8.3), pickleworm, spider mite (see Figs. 8.14, 8.15), and spotted, striped (see Figs. 8.12, 8.13), and banded cucumber beetles.

PI 299563 is resistant to melon aphid (Aphis gossypii). 'Congo' and 'Giza 1' were the most resistant of five accessions evaluated for resistance to spider mite. Several genes were found to control non-preference type resistance to spotted cucumber beetle in 'Hawkesbury' x a resistant accession. Resistance to spotted and banded cucumber beetles was due a single recessive gene.

A single dominant gene, Fwr, was responsible for resistance to the melon fruit fly (Dacus cucurbitae) in the watermelon line JI8-1. ‘Afghan’ is reported to have resistance to red pumpkin beetle (Aulacophora foveicollis), and 'Blue Ribbon' and 'Crimson Sweet' are resistant to pickleworm.

Stress

Little research has been done on stress resistance in watermelon. Water stress is an important cause of reduced yield in watermelon. It may be that some genotypes are more efficient in water use than others, but it probably will be difficult to develop highly efficient varieties since watermelon fruit have very high water content. In Israel, deep-rooted varieties are used in unirrigated desert areas.

Pollination problems are responsible for improper fruit development. It is necessary for all three lobes of the stigma to be fully pollinated if the fruit is to develop fully, and without curvature. Proper fruit development requires adequate numbers of honeybees or bumblebees during flowering, along with weather that is conducive to pollination. Bumblebees can be more effective pollinators than honeybees. Cold, rainy weather leads to poor pollen shed, and hot weather often leads to reduced bee activity. In the case of triploid hybrids, it is necessary to have up to one third of the field planted to a diploid pollenizer to assure adequate fruit development in the triploids which are male sterile.

Growers plant early in the season, often using transplants and plastic mulch (with row covers in some cases) when there is a danger of frost. Cucurbits are susceptible to chilling injury at air temperatures below 42°F. Chilling injury is a concern in watermelon because of the value of early harvested fruit. There might be chilling resistance in the watermelon germplasm collection that could be incorporated into new varieties as has been done in other cucurbits. Watermelon appears to be more chilling resistant than melon and cucumber. Symptoms of chilling are white areas on the cotyledons and white or light brown margins on the fully expanded leaves. Chilling injury is increased by a longer duration of chilling, lower temperature, high intensity of light during chilling, high wind speed during chilling, or a higher growth temperature before chilling occurs. Watermelon is thermophilic, meaning that plants have a high optimum growth temperature. Although the optimum is probably 80-90°F, temperatures above 90°F reduce growth rate, and can reduce fruit yield. Above 105°F, plants can be injured, and young leaves will be light green with yellow margins.

Measles is a condition where green-brown spots develop on the fruit surface, covering a small area or even the entire surface, and starting out as minute watersoaked areas. The spots become tan, slightly raised areas with necrotic centers. The symptoms occur when excessive guttation is encouraged by periods of high humidity or during the early fall production season when the humidity is high and the nights are cool. The fruit symptoms become evident 21-25 days after the conducive environmental conditions occur. There is usually no economic loss from the stress, and it might be controlled by reducing the amount of irrigation in the fall production season.


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Created by T.C. Wehner and C. Barrett 5 September, 1996; design by C.T. Glenn;
maintained by T.C. Wehner; last revised on 20 June, 2010