MUSKMELON AND WATERMELON PESTS IPM PRINCIPLES IMPORTANCE OF DIAGNOSIS UNDERSTANDING INFECTIOUS DISEASES Inoculum Mechanisms of Disease Spread Disease Cycles DISEASE CONTROL OPTIONS Cultural Control Disease Resistance Chemical Control MELON CROP DISORDERS Infectious Disorders Alternaria Leaf Blight Anthracnose Bacterial Fruit Blotch Bacterial Wilt Damping Off Dodder Downy Mildew Fusarium Wilt Gummy Stem Blight Powdery Mildew Root Knot Nematode Sudden Wilt Virus Diseases Noninfectious Disorders Blossom End Rot Internal Rind Necrosis Magnesium Deficiency Manganese Toxicity Molybdenum Deficiency Ozone Injury Salt Burn Arthropod Pests Aphids Cucumber Beetles Spider Mites Seed Corn Maggots Unexplained Disorders Watermelon Cross Stitch Greasy Spot Target Cluster Fusarium Fruit Rot SEED-BORNE DISEASES IN TRANSPLANT PRODUCTION FACILITIES * Richard Latin is a professor of Plant Pathology, Department of Botany and Plant Pathology, Purdue University.
Pests are biotic (living) factors that interfere with crop production. Melon crop pests in the Midwest include plant pathogens (bacteria, fungi, nematodes, and viruses), arthropod pests (insects and mites), and weeds. This guide focuses on plant pathogens, because diseases are responsible for the majority of pest-related yield reductions in melons. Arthropod pests are significant, but represent less of a threat. Moreover, the insects that warrant the most attention (cucumber beetles and aphids) are a concern mostly because they transmit bacteria and viruses that cause serious diseases.
Not all pests are addressed in this guide. Vertebrates (moles, rabbits, and birds) are pests, but their effects are generally negligible. Weeds and weed management are so important that they deserve separate treatment. Diseases and arthropod pests are not separated because management decisions are made and implemented together throughout the season.
There probably are as many interpretations of "integrated pest management" (IPM) as there are people who have given the matter serious thought. My interpretation is that IPM involves using knowledge and all possible options to control a crop disorder with the minimum of inputs, especially financial and chemical. For many crop disorders, IPM is exercised before the crop is planted by sampling soils and selecting appropriate field sites and varieties to reduce the risk of disease- or pest-related loss during the season. Other crop problems, especially those that become established and spread during the growing season, need almost constant attention from planting until harvest. These problems tend to be the most destructive and require more chemical control inputs to protect the crop. This guide focuses on those challenges that growers confront during the season and the options available to reduce their effects on the crop.
Diagnosis is the essential first step in managing crop disorders, because it is impossible to find a solution without first identifying the problem. The consequences of an incorrect diagnosis can be severe. For example, a mistake in diagnosis can result in no remedial action being taken, or inappropriate treatment. The farmer then is likely to suffer loss in yield as well as having paid for the wrong treatment. Not all outcomes of incorrect diagnoses are that extreme; however, in order to efficiently and effectively manage melon crops, farmers must be able to recognize all important crop disorders.
Becoming skillful at identifying crop problems takes experience and knowledge of characteristic symptoms of melon disorders. This guide contains color photographs that illustrate symptoms of melon disorders that occur in midwestern production areas. It is important that growers familiarize themselves with symptoms of each disorder and try to understand how symptoms of some disorders differ from others. For example, Alternaria leaf blight and anthracnose both produce brown lesions on muskmelon leaves. However, anthracnose also results in lesions on stems and fruit, but Alternaria leaf blight symptoms occur only on leaves.
I have always been an advocate of helping farmers help themselves. I believe that the most valuable solutions are those that originate closest to the source of the problem. Consider a simple example. Suppose there is an outbreak of powdery mildew in a field. If the disease is identified in the field, a remedial fungicide treatment can be applied within 24 hours and probably will be effective enough to keep the disease in check for the remainder of the season. However, if the mildew symptoms were discovered but not identified for a week or more, the disease could become firmly established in the field to the extent that managing it would require a costly, season-long effort.
The point is that in order to make the best possible decisions to fight melon diseases and disorders, growers must arm themselves with as much diagnostic knowledge as possible. It should be no surprise that the most successful farmers are those who are most capable of solving their own crop management problems.
Unlike other pests, plant pathogens cannot be seen with the unaided eye. Growers observe only the effects (symptoms) of diseases such as leaf spots, blights, wilts, etc. These circumstances contribute to a fundamental lack of understanding of the nature of plant pathogens.
Attack by plant pathogens (fungi, bacteria, nematodes, and viruses) is inevitable in commercial melon growing operations. Growers can best prepare themselves to defend against infectious diseases by understanding where the pathogens come from, how they spread, and how they survive.
This section provides an introduction to the basics of plant diseases and explains the survival and spread of plant pathogens. For growers to begin to appreciate the nature of infectious diseases, they should become familiar with terms such as primary inoculum, secondary inoculum, monocyclic disease, polycyclic disease, and the various types of pathogen dispersal as discussed below.
Inoculum is a term that will be used frequently throughout this guide, so it is important to provide a clear and thorough definition at the beginning.
Inoculum is the part of the pathogen that causes disease or creates an infection. All pathogens produce inoculum, but they usually take different forms and survive in different places.
Some fungal pathogens produce spores that are dispersed through the air and deposited on susceptible plants where they may create new infections. Others produce overwintering structures that survive in soil, by themselves, or among crop debris. Bacterial pathogens do not produce spores; instead, the bacteria themselves serve as inoculum that can overwinter with crop residue and be splash-dispersed to other plants. Virus particles, usually transmitted by other agents such as insects, represent the inoculum for virus diseases. Nematodes lay eggs in the soil or in infected roots. The eggs survive the winter, hatch in the spring and release juvenile forms of nematodes that create new infections. There are other examples, but the point is already made: Inoculum is that part of the pathogen that can create new infections.
In terms of understanding strategies for controlling diseases, it often is necessary to distinguish between primary inoculum and secondary inoculum.
* Primary inoculum is responsible for creating the initial infections among crop plants in a given season.
* Secondary inoculum is produced by infected plants during the season.
Inoculum is that part of the pathogen that has the potential to create new infections.
* Primary inoculum represents the initial disease threat to the crop.
* Secondary inoculum is responsible for the spread and increase of disease during the season.
For diseases to spread and cause significant damage to the crop, the pathogens must be dispersed from infected plants or plant material to healthy plants. Melon diseases are spread in several different ways as described below.
* Splash dispersal refers to the spread of the pathogen in splashed droplets from rain or irrigation water. Inoculum carried in a tiny water droplet is most likely to spread from one plant to a neighboring plant. Water droplets containing spores or bacteria may move a mile or more, but movement over greater distances is not very probable.
* Wind dispersal occurs when fungal spores are lifted off of lesions by air currents and transported through the atmosphere on prevailing winds. Wind-dispersed pathogens are able to spread disease over very long distances. Spread from 1-10 miles is quite probable. Spread of 100 miles or more is possible, but much less likely to occur.
* Mechanical dispersal refers to disease spread associated with general crop management. For example, spores of some soil-borne fungi may be carried with soil on farm implements that travel from one field to another. Nematodes also are dispersed mechanically. As a general rule, mechanical dispersal is more of a concern in root diseases than in diseases that destroy vines and foliage.
* Insect vectors are insects that acquire and transmit plant pathogens. Aphids often serve as vectors for virus diseases, and cucumber beetles are vectors of the bacterial wilt pathogen.
A disease cycle is the chain of events that occurs during disease development. These events include the production of primary inoculum, infection of the host plant, growth and increase and dispersal of the pathogen, decay of the plant or plant materials, and survival of the pathogen. As discussed previously, primary inoculum is responsible for the initial infections that occur in the spring. After infection occurs, the pathogen normally grows or colonizes plant tissue at various rates, depending on the nature of the disease and the environmental conditions. As the pathogen colonizes host tissue, the plants express symptoms such as leaf spots, wilting, abnormal growth, etc. and produce more inoculum (bacteria, spores, etc.) that may or may not be dispersed throughout the field. After diseased plants or plant materials decay, the pathogen may survive in association with the debris in the soil throughout the winter. The survival capacities of many plant pathogens are not well understood, but, for the sake of this discussion, they can be grouped into three categories. NONLOCAL SURVIVORS are unable to overwinter in midwestern climates (cucurbit downy mildew is a good example). LOCAL-RESIDUE SURVIVORS overwinter in local fields, but always in association with infested crop residue (Alternaria leaf blight is an example). LOCAL-SOIL SURVIVORS produce weather-resistant structures that can survive alone in soils, without association with infested crop debris (Fusarium wilt of muskmelon and watermelon, for example, produce spores that survive alone in the soil).
Understanding disease cycles is important in formulating disease control strategies. Infectious diseases can be classified according to the number of disease cycles that occur in a growing season. For example, the chain of events in a Fusarium wilt disease cycle occurs only once (Figure 1). Primary infection occurs after roots growing in the soil contact Fusarium spores. Once infection is established, the pathogen colonizes the vascular system of the roots and stem, resulting in wilt, collapse, and decay of the plant. Local-soil surviving spores are released into the field and provide the primary inoculum for the next crop of susceptible melons. The spores are not dispersed to cause new infections on neighboring plants. Because the cycle of events occurs only once, Fusarium wilt is classified as a monocyclic disease.
In contrast, polycyclic diseases are characterized by the occurrence of many infection cycles throughout the season. For many diseases, especially foliar diseases, the process of infection, colonization, production of secondary inoculum, dispersal of secondary inoculum, and the establishment of new infections occurs almost continuously throughout the season. Gummy stem blight is a polycyclic disease, and its disease cycle is illustrated in Figure 2. Primary inoculum may be seed-borne, although in midwestern fields it usually survives in association with crop debris. Primary infections occur on young seedlings in the spring. Under cool spring conditions the gummy stem blight fungus grows slowly through melon leaves and stems. Lesions develop more rapidly as temperatures increase. Mature lesions produce spore-bearing structures called pycnidia, which can spew tens of thousands of spores onto the lesion surface under moist conditions. The spores are splashed to neighboring plants (or fields) during periods of rainfall or irrigation and create new infections. The new infections result in new lesions, which produce new spores that are splash-dispersed to more plants where more infection cycles will occur, and so on.
Figure 1. The chain of events in a Fusarium wilt disease cycle occurs only once.
These two types of disease cycles represent generalizations, i.e. not all diseases can be pigeon-holed into one category or the other. However, a large majority of infectious diseases are easily classified as monocyclic or polycyclic. The classification is very helpful in illustrating disease control strategies. For monocyclic diseases, most of the crop damage is a result of primary infection, and therefore control strategies are aimed at eliminating or reducing primary inoculum. For polycyclic diseases, most of the crop damage is due to numerous secondary cycles, and therefore control strategies are targeted towards reducing the number of secondary cycles and/or the rate at which they occur.
Figure 2. Gummy stem blight is a polycyclic disease.
This section introduces the principles of disease control. It is intended to describe the three major disease control practices, how they work, and where their use is appropriate.
Specific chemicals or varieties used for disease control are not discussed in this book. Such information changes each year and is normally available in publications prepared by state extension specialists.
The objective here is to provide an understanding of how various control practicies affect disease cycles. This knowledge will help you make better decisions regarding the use of specific disease control chemicals, varieties and other control options.
Cultural control comprises those options available to melon growers that do not involve the application of chemicals or the use of disease-resistant varieties. Fall plowing, crop rotation, and sanitizing equipment all can be classified as cultural control options. Cultural methods lessen the threat of disease by reducing the amount of primary inoculum available for infection in the spring. For example, fall plowing buries and hastens the decomposition of crop residue. Because many plant pathogens must be associated with crop residue to survive until favorable conditions return, any reduction in the amount of residue will result in a decrease in the pathogen population that survives the winter.
Disease resistance is an inherited trait that results in a reduction in disease incidence and/or severity. Resistance normally is the result of years of plant breeding and selection in an effort to incorporate resistance genes into a horticulturally acceptable variety.
Resistance is described as being complete or partial. Complete resistance is expressed when infection by the pathogen is prevented and no disease symptoms occur. For example, several muskmelon varieties grown in southwestern Indiana possess complete resistance to the Fusarium wilt pathogen. These varieties can be raised in fields with a long history of wilt problems without succumbing to the disease.
Complete resistance usually is developed against common races or strains of a pathogen. Because pathogen populations are constantly changing at different rates in different regions, genes that confer complete resistance may not be universally effective. Varieties that express complete resistance against local strains of a pathogen may be susceptible in other regions.
Partial resistance is expressed in situations where infection by a pathogen occurs, but the disease progresses slowly, often resulting in less crop damage when compared to a standard susceptible variety. This type of resistance usually is identified in the field where observers notice that one variety may sustain less disease than another over the entire season. Partial resistance alone often is not sufficient to eliminate yield losses due to disease; however, when combined with other disease control strategies (such as a few timely fungicide sprays) losses are likely to be negligible or reduced substantially.
Resistant varieties of either type should be used wherever possible. It is a practice that is environmentally sound and economically prudent and will contribute to a long-term reduction in disease pressure in individual fields and entire regions.
Unfortunately, no muskmelon or watermelon varieties currently are available with resistance to all important diseases in a given region. Resistance to one or two diseases has been incorporated into a few varieties. Growers should consult objective appraisals of varietal performance against disease before selecting varieties advertised as disease resistant.
Sometimes the term "tolerance " is substituted incorrectly for partial resistance. In fact, that term often is misused in seed catalogs. Tolerance to disease occurs when two varieties suffer the same amount of disease, but one variety sustains significantly greater yield loss. The variety that sustains proportionately less yield loss is said to be tolerant to the disease in question. The phenomenon of "tolerance" has not been demonstrated in melons or any other fruit or vegetable crop. Tolerance to disease is most often observed by researchers involved in breeding for disease resistance in grain crops.
Chemical disease control involves the application of pesticides to reduce the effects of pathogen populations on crop yields. Fumigants and nematicides often are used to keep nematode populations in check. Fungicides and copper compounds are applied repeatedly during the growing season to control foliar diseases. This discussion will focus on fungicides, because decisions regarding their use must be made regularly throughout the season. General categories of fungicides rather than specific fungicide products will be discussed because specific products change each year and information concerning their use normally is prepared by state extension personnel.
Fungicides are classified into two major groups, protectant fungicides and systemic fungicides.
PROTECTANT FUNGICIDES are designed to provide a chemical barrier between the plant surface and the pathogen. They prevent infection from occurring by killing spores before or after they germinate. This mode of action does not prevent all infections, but drastically reduces the number of secondary disease cycles that can occur. The result is a significant reduction in the rate of epidemic progress so that the effect of the disease on yield is greatly reduced. Characteristics of protectant fungicides that affect how they work are discussed below.
SYSTEMIC FUNGICIDES are absorbed by the plant and are designed to kill or severely retard existing infections. Because toxic concentrations can remain in the plant for more than a few days, systemic fungicides also provide some protection against new infections. These fungicides usually are applied less frequently and at lower rates than protectant fungicides. Characteristics of systemic fungicides that affect how they work are discussed below.
Alternaria leaf blight is a much greater threat to muskmelons than watermelons. The disease is caused by a fungus (Alternaria cucumerina) that can rapidly defoliate plants, causing reductions in bulk yield. Melons on defoliated vines ripen prematurely and result in lower quality fruit compared to melons produced on healthy vines. Yield losses greater than 50% will occur in situations where the disease is established early in the season and weather conditions throughout the summer are favorable for disease increase and spread.
Alternaria infections occur only on leaves. Petioles, stems, and fruit are not directly affected by the pathogen (Fig. 3). Lesions begin as tiny, tan or brown spots that may appear watersoaked on the underside of leaves. Older lesions are generally round, brown, and may be surrounded by a halo of yellow tissue (Fig. 4). Within the brown areas of Alternaria lesions are characteristic concentric circles that resemble the growth rings of a tree. (Fig. 5).
Disease Characteristics Disease cycle: * polycyclic Source of primary inoculum: * fungal structures surviving on crop debris Secondary inoculum: * spores produced on infected plants Spread: * wind dispersal and splash dispersal Disease Control Disease resistance: * Acceptable levels of resistance are not yet available in muskmelon varieties. Cultural control: * Rotations of 2-4 years and fall tillage of severely affected fields will help reduce the amount of primary inoculum that threatens the next melon crop. Chemical control: * Repeated applications of protectant fungicides are necessary for reducing disease-related loss, especially in fields with a history of the disease. * Weather-based spray advisories may be available to help schedule fungicide treatments.
Anthracnose is caused by a fungal pathogen (Colletotrichum orbiculare) that can affect both muskmelons and watermelons. Severe anthracnose epidemics can result in near total losses. Rapid defoliation of vines reduces bulk yields. Fruit infection results in unsalable melons.
Anthracnose infection can occur on stems, leaves, and fruit. Leaf symptoms include irregularly shaped, dark brown lesions. Lesion growth often is limited by leaf veins, giving the lesion an angular or jagged appearance (Figure 6). As lesions expand and their diameter approaches 1/2 inch, the dead brown tissue often cracks and may leave a split or a hole in the lesion. Muskmelon stem infections result in sunken, tan-colored cankers (Figure 7). Lesions on watermelon stems are somewhat oval and tan colored, usually with a brown margin (Figure 8). Fruit lesions are round, sunken, and orange- or salmon-colored and most often occur on the sides of infected fruit of muskmelon (Figure 9), and watermelon (Figure 10). Anthracnose symptoms on melon seedlings are addressed in the chapter on Seed-borne Diseases in Transplant Production Facilities.
Disease Characteristics Disease cycle: *polycyclic Source of primary inoculum: *fungal structures surviving on crop debris *contaminated seed Secondary inoculum: *spores produced on infected plants Spread: *splash dispersal Disease Control Disease resistance: *Partial resistance has been reported in a few commercial varieties, but will not provide acceptable control without chemical protection. Cultural control: *Rotation and tillage options will help reduce the disease threat in subsequent years, but will not provide acceptable control in fields with a history of the disease without chemical protection. Chemical control: *Repeated applications of protectant fungicides are necessary for reducing disease-related loss, especially in fields with a history of disease. *Use of partially resistant varieties and implementation of appropriate cultural control options will contribute to more efficient and effective chemical control.
Bacterial fruit blotch was introduced to midwestern melon production areas in 1989 with contaminated seed of a certain watermelon variety. It is suspected that contaminated seed also was responsible for the fruit blotch epidemics of 1992. Early season outbreaks can result in total losses. Fields near severely affected crops can suffer 5-50% loss, depending on environmental conditions and the crop growth stage at which fruit blotch becomes established.
The characteristic symptom of bacterial fruit blotch is the dark olive green stain or blotch that occurs on the upper surface of infected fruit (Figure 11). Initially the blotch is about the size of a quarter, and then rapidly expands so that much of the fruit surface is covered with the lesion in 7-10 days (Figure 12). As the blotch increases in size, the area around the initial infection site turns brown. The epidermis of the rind ruptures (cracks) in advanced stages of lesion develop ment and frequently oozes a sticky, clear-amber colored substance (Figure 13). Fruit lesions rarely extend into the flesh of the melon (Figure 14); secondary rotting organisms are responsible for the ultimate decay and collapse of fruit. Bacterial fruit blotch also attacks muskmelon fruit, often producing watersoaked pits (partially resembling anthracnose symptoms) on the fruit surface (Figure 15).
The fruit blotch bacteria also infect leaves, although foliage surrounding infected fruit may appear healthy to the untrained eye. Leaf lesions are small, dark brown, somewhat angular, and generally inconspicuous (Figure 16). When viewed from the bottom of the leaf, the margins of the lesions appear watersoaked, especially in wet or humid weather.
Symptoms on seedlings are discussed in the chapter on Seed-borne Diseases in Transplant Production Facilities.
Disease Characteristics Disease cycle: * polycyclic Source of primary inoculum: * infested (contaminated) seed * infested crop residue Secondary inoculum: * bacteria produced on the surface of lesions Spread: * splash dispersal Disease Control Disease Resistance: * Partial resistance may occur in some watermelon varieties. Most varieties are very susceptible. Cultural control: * Infested fields must be plowed in the fall and planted to grain crops where herbicides will control volunteer watermelons in the following season. Fields should be rotated out of cucurbits for three years or more. Follow greenhouse sanitation procedures as outlined in the chapter on Seed-borne Diseases in Transplant Production Facilities. Chemical control: * Copper sprays applied at 5- to 7-day intervals may reduce the severity of epidemics.
Bacterial wilt is a common disease of muskmelons, but does not affect watermelons. The bacterial pathogen, Erwinia tracheiphila, multiplies within the vascular system of infected plants, causing rapid wilt and collapse of vines. The pathogen is transmitted by cucumber beetle vectors. Losses due to bacterial wilt can range from 10-20% in a disease-favorable season.
Initial symptoms of bacterial wilt include flagging or wilting of leaves on one or more vines (Figure 17). Symptom development proceeds rapidly; entire plants may collapse and die within a few days (Figure 18). Most of the loss caused by bacterial wilt occurs up to three weeks before harvest begins and coincides with springtime increases in cucumber beetle populations. In some seasons, wilt and collapse continues to occur after harvest begins. A diagnostic test for bacterial wilt can be performed in the field by cutting a wilted vine close to the main stem, rejoining the cut surfaces, then slowly drawing the sections apart. Bacterial wilt can be positively diagnosed if a thin strand of slime extends between the two sections (Figure 19).
Disease cycle: * polycyclic Source of primary inoculum: * adult cucumber beetles that emerge in mid-spring Secondary inoculum: * bacteria produced in infected plants Spread: * the bacteria are transmitted from infected plants to healthy plants by cucumber beetles Disease Control Disease resistance: * No muskmelon varieties are resistant to bacterial wilt. Watermelons are not affected by the disease. Cultural control: * Cultural practices appear to have no effect on disease development. Chemical control: * Bacterial wilt control is directly related to control of cucumber beetles. Soil-applied insecticides and repeated applications of foliar contact insecticides are necessary for adequate disease control.
Damping-off is a disease that affects melon seedlings at their earliest stages of growth. Several soil-borne fungi may be associated with damping-off, but it most often is caused by a species of Pythium. Losses can be very severe. Infections result in reduced stands in seed flats or rapid wilting and death of young seedlings.
Damping-off may occur before or after seedlings emerge from the soil. In the case of pre-emergence damping-off, the pathogen infects seeds as they germinate. As infection progresses, the seeds rot and eventually disintegrate. As a result of pre-emergence damping-off, poor stands become apparent days or weeks later (Figure 20).
Post-emergence damping-off most often is observed in seed flats or among transplants. The Pythium fungus infects roots and stems near the soil surface. Infections result in water-soaked stems that usually collapse within 24 to 48 hours (Figure 21).
Disease Characteristics Disease cycle: * monocyclic Source of primary inoculum: * soil Secondary inoculum: * mold from diseased roots and stems Spread: * limited spread occurs as mold from infected plants grows through the soil and contacts roots of neighboring seedlings * any mechanism for transporting soil will contribute to the spread of Pythium Disease Control Disease resistance: * None. Cultural control: * Losses attributed to damping-off might be reduced by manipulating the environment so that the seedling escapes infection. Specific options include the following: --Plant seeds shallow, preferably in a commercially prepared soilless potting medium. --Irrigate in the morning. --Avoid excess nitrogen fertilizer. Chemical control: * Fungicidal seed treatments will result in good damping-off control.
Dodder is a parasitic plant that can severely reduce melon yields, but it rarely occurs in midwestern melon fields. There appears to be no difference between watermelons and muskmelons in their susceptibility to dodder infection. Incidence of dodder infestation appears to be greater in melon crops raised on dark, sandy soils.
Dodder infestations are readily apparent as distinct bright yellow clusters within fields (Figure 22). Closer inspection of affected plants reveals the dense mat created by the vine-like dodder plant (Figure 23). Dodder vines wrap around melon leaves, petioles, and stems and produce penetration structures that pierce the outer layer of plant cells and suck water and nutrients from the melon plant (Figure 24). The bright yellow color changes to a dull yellow or tan as the dodder matures and produces many tiny, seed-bearing flowers.
Disease Characteristics Disease cycle: * monocyclic Source of primary inoculum: * seeds in soil Secondary inoculum: * none Spread: * any mechanism that moves soil between fields Disease Control Disease resistance: * None. Cultural control: * Many crop plants are parasitized by dodder, but legumes (such as alfalfa and clover) and melons appear to be most prone to infestations in the Midwest. Rotation with less susceptible crops should reduce the incidence of dodder. Chemical control: * Some pre-emergence herbicides are effective in preventing seed germination and subsequent plant establishment in the spring.
Downy mildew is a disease that rarely results in economic damage to midwestern melon crops. The pathogen is a fungus, Pseudoperonospora cubensis , that does not produce survival structures in the north, and overwinters as active colonies in Gulf Coast states. The pathogen accompanies cucurbit production as it progresses northward each spring. Usually by the time downy mildew becomes established in the Midwest, melon harvest is completed, or in its final stages.
Downy mildew is easily confused with other melon disorders because it only affects leaves. Initial symptoms include large angular or blotchy shaped yellow areas visible on the upper surface (Figure 25). As lesions mature, they expand rapidly and turn brown (Figure 26). The under surface of infected leaves appears watersoaked. Upon closer inspection, a purple-brown mold becomes apparent on the under surface (Figure 27). Small spores shaped like footballs can be observed among the mold with a 10x hand lens. In disease favorable conditions (cool nights with long dew periods) downy mildew will spread rapidly, destroying leaf tissue without affecting stems or petioles (Figure 28).
Disease Characteristics Disease Cycle: * polycyclic Source of primary inoculum: * active colonies in southern states Secondary inoculum: * spores produced on infected plants Spread: * wind dispersal Disease Control Disease resistance: * Partial resistance has been reported in a few commercial varieties. Check with seed company representatives. Cultural options: * Because the downy mildew pathogen does not overwinter in midwestern fields, crop rotations and tillage practices do not affect disease development. The pathogen tends to become established in late summer. Therefore, planting early season varieties may further reduce the already minor threat posed by downy mildew. Chemical control: * Fungicides that are effective against Alternaria leaf blight, gummy stem blight, and anthracnose also protect against downy mildew. Eradicant fungicides are labeled for use against cucurbit downy mildew, but are recommended only after diagnosis of this disease has been confirmed.
Fusarium wilt affects both muskmelons and watermelons. Although the common name of the disease is the same for both types of melons, different pathogens are involved. Fusarium oxysporum f. sp.melonis causes Fusarium wilt of muskmelons, and Fusarium oxysporum f. sp. niveum causes Fusarium wilt of watermelons. Losses to Fusarium wilt have been reduced substantially over the past 10-15 years with the introduction of resistant varieties. However, the disease occurs to some extent each year in locations that have had a history of wilt, especially in traditional sandy soil production areas. Yield reductions in severely affected fields can approach 50%.
Fusarium wilt is most readily identified after young plants begin to produce runners, but before the initial harvest. Affected plants appear in clusters and are often (but not always) located in low areas of a field where drainage is less than optimal. The Fusarium pathogens cause infected plants to wilt slowly. Leaves close to the crown of the plant usually wilt first. Chlorosis, or yellowing, of the crown leaves also may occur (Figure 29). Close inspection of the lower stems of infected plants reveals narrow brown streaks or lesions along the vines. Affected stems also appear cracked and exude a red, brown, or black gummy substance (Figure 30). Also, because Fusarium wilt affects the plant's vascular system, the vascular bundles of infected plants assume a brown discoloration (Figure 31).
Disease Characteristics Disease cycle: * monocyclic Source of primary inoculum: * resilient spores that survive in soils for indefinite periods of time Secondary inoculum: * none Spread: * mechanical spread with soil on farm implements from year to year Disease Control Disease resistance: * Muskmelon and watermelon varieties with excellent resistance to Fusarium wilt are available. Rely on extension publications and seed catalogs to identify appropriate melon varieties. Cultural control: * Long rotations of non-cucurbit crops will help to slowly reduce Fusarium populations in soil. Substantial losses will occur if susceptible varieties are planted into fields with a history of the disease, even though a long rotation had been employed. Standard three- to four-year rotations also are recommended even if resistant varieties are used. Chemical control: * None.
Gummy stem blight (GSB) is caused by a fungus (Didymella bryoniae) that attacks muskmelons, watermelons, and other cucurbits. It causes the disease known as "black rot" on pumpkins and squash. Yield loss due to GSB occurs as a result of rapid defoliation of vines and fruit infection and subsequent decay.
Symptoms of GSB on leaves often appear as irregularly shaped brown areas that often first occur in the "palm" of the leaf, where it attaches to the petiole (Figure 32). Infected petioles and stems first appear watersoaked. As the infection progresses, an elongated, tan-colored lesion develops. Mature GSB lesions appear corky and cracked and often exude an orange-red-brown gummy substance (Figure 33). The key diagnostic feature of GSB is the presence of small black fungal structures called pycnidia embedded in the diseased tissue. Pycnidia are smaller than a period printed on this page and often occur in groups or clusters within the lesion (Figure 34). A 10x hand lens should be used to view the pycnidia clearly. Do not confuse GSB stem lesions with those caused by Fusarium wilt! Both diseases cause stem lesions that may exude the orange-red-brown fluid. A cross-section of infected vines illustrates the difference in symptoms caused by the two diseases. The vascular bundles of wilt-infected plants appear discolored; GSB-infected stems exhibit an apparently healthy vascular system (Figure 35).
Gummy stem blight also can occur on seedlings raised in transplant production facilities. Symptoms on seedlings and various control options are discussed in the chapter on Seed-borne Diseases in Transplant Production Facilities.
Disease Characteristics Disease cycle: * polycyclic Source of primary inoculum: * fungal structures surviving on crop debris * contaminated seed Secondary inoculum: * spores produced on infected plants Spread: * splash dispersal Disease Control Disease resistance: * There appear to be no commercially acceptable watermelon or muskmelon varieties with adequate resistance to GSB. Cultural control: * Implementing cultural control options alone will not result in satisfactory control of GSB. However, employing options such as fall tillage of severely affected fields, rotating fields with nonsusceptible crops for at least 2 years, and avoiding fields with a history of the disease may contribute to more effective and efficient chemical control. Chemical control: * Apply protectant fungicides at 7- to 14-day intervals beginning when vines of adjacent plants touch within rows. * Begin fungicide applications sooner if infection was discovered in transplant production facilities. * Fungicides for GSB control also are effective against Alternaria leaf blight, anthracnose, and (to some extent) downy mildew.
Powdery mildew, caused by the fungus Sphaerotheca fuliginea, is a major disease of muskmelons in the Midwest. The disease has been reported on watermelons in southern states, but does not occur on watermelons in Indiana. The powdery mildew pathogen does not infect melon fruit. However, severe outbreaks will result in rapid defoliation of vines, reduced fruit per acre, and poor quality fruit.
Of all the disorders of muskmelons, powdery mildew is the simplest to diagnose. The first obvious signs of a powdery mildew outbreak are a few small clusters of affected plants scattered throughout a field (Figure 36). Clusters of diseased plants normally appear shortly before harvest begins if no fungicides for mildew control are applied. Closer inspection of individual plants reveals the characteristic white mold of powdery mildew infection (Figure 37). The mold occurs on both sides of the leaves and often results in an upward cupping effect of leaves sustaining severe mildew infection (Figure 38).
Disease Characteristics Disease cycle: * polycyclic Source of primary inoculum: * spores surviving on crop debris Secondary inoculum: * spores produced on infected plants Spread: * wind dispersal Disease Control Disease resistance: * Effective mildew resistance can be incorporated into muskmelon varieties. Check with seed company representatives. Cultural control: * Rotation and tillage options will have only a minor effect on powdery mildew control. Chemical control: * Effective systemic fungicides are available. Initial sprays should be applied approximately 10 days before harvest. * Subsequent sprays (1 or 2) should follow at 14- to 21-day intervals.
Root knot nematodes are microscopic worms that inhabit sandy soils and can parasitize the roots of almost all vegetable crops. As nematodes feed and multiply within melon roots, they retard uptake of water and growth of vines. Losses in fields that are heavily infested with root knot nematodes can approach 50%. Nematode problems normally are more severe in hot dry summers.
Plants affected by root knot nematodes usually first appear in clusters on side-hills of fields with sandy soils. Plants whose roots are infected shortly after transplanting will appear stunted throughout the season. Plants infected later in the season normally wilt as soon as they are exposed to the slightest water stress (Figure 39). The diagnostic feature of root knot nematode infection is the presence of galls on roots of affected plants. Severely affected plants may have galls as large as 1 inch in diameter (Figure 40).
Disease Characteristics Disease cycle: * monocyclic Source of primary inoculum: * hard-shell nematode eggs that survive in soil indefinitely Secondary inoculum: * none Spread: * mechanical spread with soil on farm implements Disease Control Disease resistance: * No melon varieties are resistant to root knot nematode infection. Cultural control: * Long rotations with grain crops may help maintain reduced nematode population levels. Because eggs can survive indefinitely, root knot nematodes always will be a threat in fields with a history of the disease. Chemical control: * Fumigants or nematicides are necessary for melon production in fields with a history of root knot problems.
Sudden wilt is a relatively new disease of watermelons in Indiana. Root decay indicates that the disorder is infectious. However, it is currently suspected that cultural factors contribute significantly to wilt development. The use of plastic mulch and irrigation appear to increase wilt incidence. Within the past five years, losses observed in severely affected fields have approached 80%. Plants affected by sudden wilt yield few, if any, fruits, and melons from wilted vines have poor quality. To date, this disease has been observed on watermelons, but not muskmelons.
Sudden wilt first appears in low-lying areas of affected fields (Figure 41). Vines on individual plants wilt rapidly; older leaves may turn yellow before they collapse (Figure 42). No other distinctive above-ground symptoms appear to be associated with the disease. Affected areas enlarge over time (Figure 43); sudden wilt can spread to higher, well-drained areas of a field. Roots of wilted plants are typically discolored (dark red-brown) and in various stages of decay. Roots of severely wilted plants are thoroughly rotten (Figure 44).
The exact cause of sudden wilt is not known. It is presumed that environmental and cultural factors predispose roots to infection by several soil-borne fungi acting alone or in combination. The disease spreads most quickly within rows, leading to the suspicion that the dense root growth and elevated soil moisture levels beneath plastic mulch allow the pathogen to traverse a continuous bridge of susceptible tissue in favorable environmental conditions.
Disease Control Disease resistance: * All watermelon varieties are susceptible. The disease does not yet appear to affect muskmelons. Cultural control: * Standard rotational and other production tillage practices are required for profitable melon production. * Because high moisture levels and plastic mulches are highly correlated with incidence of sudden wilt, growers are warned against liberal use of irrigation, especially early in the season while the rate of vine growth is most rapid. Chemical control: * None
Virus diseases of muskmelons and watermelons may be caused by any of five different pathogens: cucumber mosaic virus (CMV), papaya ring spot virus - watermelon strain (PRSV-W), squash mosaic virus (SQMV), watermelon mosaic virus 2 (WMV-2), and zucchini yellows mosaic virus (ZYMV). CMV and SQMV occur rarely, although the effects of SQMV can be especially severe because the virus can be seed-borne. ZYMV is identified occasionally and also can result in severe losses. Casual surveys during the past 10 years in Indiana indicate that WMV-2 and PRSV W are the most common virus diseases. Muskmelon crops appear to suffer greater losses to those two viruses than watermelons.
The extent of crop loss due to virus disease is highly correlated with the crop growth stage at which the virus becomes established in the field. Melon plants infected early in their development (near or before the time of flowering) are severely affected and produce few (if any) fruits. However, plants infected four or more weeks after harvest begins may not show any yield loss. Late-season melons are especially prone to losses associated with virus diseases.
Early season infections usually result in stunted plants with abnormal shape and color. Symptoms on plants infected later in the season are usually discovered in leaves. Virus symptoms first appear on new growth, shortly after infection occurs. The most common symptoms of virus-infected melon plants are abnormally shaped and colored leaves. SQMV, a seed-borne virus that can spread rapidly in a transplant production facility, produces mottled leaves with spiny margins (Figure 45). WMV-2 and PRSV-W usually appear later in the season and produce symptoms on leaves and fruit. Infected leaves have an abnormal shape and exhibit a mosaic of light and dark green tissue (Figure 46). Melons from infected vines often are irregularly shaped and have an abnormal or incomplete net (Figures 47 and 48).
Disease Characteristics Disease cycle: * polycyclic Source of primary inoculum: * infected weed hosts in fencerows, wooded and non-cultivated fields * SQMV is seed-borne Secondary inoculum: * virus particles produced in infected plants Spread: * insect vectors (especially aphids) * mechanical operations that disturb plants and bruise leaves and vines Disease control Disease resistance: * None, although watermelons tend to be affected less than muskmelons. Cultural control: * Avoid planting late-season melons (especially muskmelons) adjacent to early melons. * Keep transplant production facilities weed free. Also, do not raise flowers or other ornamentals in melon transplant houses. * Control weeds within and around fields. Chemical control: * Attempts to control insects for virus disease control may be futile, because insects may transmit the virus before insecticides are effective.
Blossom end rot is a physiological disorder of watermelon caused by calcium deficiency in fruit. It is not associated with soil contact or with damage to other plant parts. Blossom end rot occurs frequently after plants have been exposed to severe drought stress. Watermelon varieties differ in the extent to which they exhibit blossom end rot. In general, long watermelon varieties (Jubilee- and gray types) are more prone to this disorder. However, under environmental conditions that favor blossom end rot, fruit of all varieties may show symptoms.
Symptoms first appear as small, light brown spots at the blossom end of immature fruit. As affected melons grow, spots can enlarge rapidly to form dark, sunken, leathery lesions (Figures 49 and 50). Lesions are generally dry and can be as large as the diameter of the fruit. A soft, secondary wet rot may develop if affected areas of fruit are invaded by decay fungi and bacteria.
Although blossom end rot is the result of a calcium deficiency in fruit, environmental conditions that interfere with uptake and availability of water and nutrients contribute greatly to symptom expression. Such conditions include water stress (especially where wide fluctuations in soil moisture occur) , excessive salinity, and root damage from infectious diseases. Excessive nitrogen fertilizer also can contribute to blossom end rot by promoting vigorous vine growth and depleting available calcium in the soil.
Internal rind necrosis is noninfectious and appears to affect only watermelons. It seems to occur very sporadically in the Midwest. Characteristic symptoms include a corky, red-brown layer of tissue that occurs on the inside of the rind of affected fruit (Figures 51 and 52). Experienced observers can detect affected melons by the very subtle knobbiness that is visible from the exterior of affected fruit.
Not much is known about the nature of internal rind necrosis. Some reports associate the appearance of symptoms with drought stress. I have observed that in affected fields, the initial harvest yields a much greater percentage of symptomatic fruit than subsequent harvests. It is not known whether some watermelon varieties are less prone to the problem. Some reports indicate that pathogenic bacteria are involved in symptom development. However, my work in the early 1990s (supported by other scientists in eastern states) showed no evidence of bacterial infection, either as a primary or secondary contaminant. Until more is learned about the disorder, I am inclined to treat it as a noninfectious disorder that is related to drought stress.
Magnesium deficiency is a noninfectious disorder that occurs in sandy soils with low (acid) pH and/or marginal soil magnesium concentrations (less than 70 ppm). It appears to be a more serious threat to muskmelons than watermelons. Losses can be severe, especially on very sandy hilltops where nutrient and chemical imbalances occur.
Symptoms of magnesium deficiency usually first appear several weeks before harvest, when vines are growing rapidly and fruits begin to increase in size and weight. Experienced observers first notice a gray-green discoloration of interveinal tissue on leaves at the crown of the plant (Figure 53). The interveinal discoloration expands and turns brown or tan over time (Figure 54). In advanced cases of magnesium deficiency, much of the tissue disintegrates, leaving what resembles the skeleton of the leaf at the crown of the plant (Figure 55).
Magnesium deficiency can be easily managed by testing soils regularly and amending with dolomitic lime when appropriate. A soil acidity level of pH 6.5 is considered optimum for melon production. Attempts to rescue affected plants with foliar applications of magnesium sulfate usually are not effective.
Manganese toxicity can have serious effects on both muskmelons and watermelons. This noninfectious disorder occurs in darker sandy soils, often in areas where run-off water travels through a field, and always is associated with acid soils (pH less than or equal to 5.8). Excess soil acidity allows elemental manganese that is normally bound to soil particles to be released and taken up into the plant in very high (toxic) concentrations. Losses to manganese toxicity can be severe, especially in muskmelon crops.
Evidence of manganese toxicity usually appears shortly before harvest, although symptoms can be recognized earlier by experienced observers. Crown leaves of plants with heavy fruit loads assume an unhealthy, pale green cast. Close inspection of leaves suffering from manganese toxicity reveals tiny lesions (approximately the size of a small pin-hole) surrounded by yellow halos (Figure 56) . The lesions occur in clusters between the veins of affected leaves. This characteristic symptom is best observed by viewing the leaf in front of the sun or another source of light. The pin-hole lesions exhibit watersoaked margins when observed from the under surface (Figure 57). As the lesions mature, they coalesce and often turn brown (Figure 58). The watersoaked lesions, the apparent decline of the crown leaves, and the clustered distribution of affected plants across a field often result in manganese toxicity being confused with several infectious diseases.
Losses caused by manganese toxicity can be avoided by maintaining soil acidity levels between pH 6.0 - 6.5. Attempts to reverse the effects of manganese toxicity by spreading hydrated lime over the field have not always had satisfactory results.
Molybdenum deficiency is most likely to affect muskmelons grown in darker sandy soils with acidity less than pH 6.0. Muskmelon losses in the range of 10-30% have been attributed to molybdenum deficiency. Watermelons do not appear to be affected.
Signs of molybdenum deficiency first appear shortly after young plants recover from transplant shock. Figure 59 shows a comparison of symptomatic plants (light green color) and a few rows of later-planted seedlings that have yet to exhibit symptoms. Leaves of affected plants become pale green or slightly yellow (chlorotic) between the veins (Figure 60). As symptoms progress, interveinal leaf tissues exhibit a distinct chlorosis, and marginal leaf tissues assume a burnt, brown appearance (Figures 61 and 62). Most symptomatic leaves occur near the crown of the plant.
Maintaining fields with near neutral soil acidity (pH 6.0-6.5) should help to avoid molybdenum deficiency. Foliar treatments of sodium molybdate have resulted in a reversal of symptom progression and a resumption of normal growth. Excess molybdenum can be harmful to melon plant growth and to the growth of rotational crops. Therefore, diagnosis should be confirmed by an expert before remedial treatments are applied.
Ozone is an air pollutant that typically occurs in high concentrations during hot, humid days that are characteristic of midwestern summers. High concentrations of ozone interfere with the plant's gas exchange functions. Losses caused by ozone damage to muskmelon vines probably are negligible. Some watermelon varieties are more sensitive to ozone. However, the stress applied by high ozone concentrations is only part of a complex of weather-related stresses that often occur during the heat of the summer. It is important to be able to recognize ozone damage so that this noninfectious disorder is not mistaken for something more serious.
Ozone damage is most evident after several consecutive days of hot, humid weather. The pattern of symptom development often is uniform, that is, all or most plants in the field show signs of the disorder. However, some plant growth and crop management factors may result in symptoms in some parts of a field, but not in others. Symptoms usually appear on the crown leaves of vigorous, rapidly growing plants with heavy fruit loads. Ozone has a direct effect only on melon leaves, causing the epidermis of the upper surface of leaves to separate from other leaf cells. Air fills the empty space below the epidermis and the tissue between the leaf veins appears white (Figure 63). The underside of the same leaf shown in Figure 63 is pictured in Figure 64. Notice that the underside of the leaf appears healthy. Ozone damage is easily recognized because, unlike other crop disorders, it does not produce symptoms on the undersurface of leaves, except in unusually severe and advanced cases of damage.
Ozone injury can be limited by crop management practices that tend to reduce other environmental stresses on melon plants. Hybrid watermelons may be less susceptible to ozone damage.
Salt burn is a noninfectious disorder that affects muskmelons more than watermelons. Salt deposits that accumulate around leaf margins can have a toxic effect on gas exchange pores (hydathodes) located at leaf tips and edges. Salt accumulation often is associated with foliar applications of nutrient solutions and/or pesticides. Copper sprays often result in distinct bands of yellow tissue around leaf margins (Figure 65).
Yield losses may occur where salt burn is severe. Some reports indicate that blossoms and young fruit are aborted after exposure to high concentrations of copper fungicides.
Aphid infestations can cause injury and loss to midwestern watermelons, but rarely affect muskmelons. Aphids also serve as vectors that transmit infectious viruses (see virus diseases, pages 47) that can result in losses that exceed 50% of the crop. Aphid and virus problems can be expected on late-season melon crops, especially during hot, dry summers.
Severe outbreaks of aphid infestations are easily identified and tend to occur in clusters. Initial signs of aphid injury appear as a downward twisting of affected leaves (Figure 66). The aphids feed in colonies on the undersurface of leaves (Figure 67). Honeydew that they excrete is deposited onto leaves in the lower canopy of the crop, giving some leaves a very wet or shiny appearance (Figure 68). The honeydew also causes stickiness on fruit surfaces and contributes to unattractive, lower quality melons.
An assortment of beneficial insects feed on aphids in midwestern melon fields. Rapid increases in aphid populations often are associated with the use of insecticides that kill natural enemies of aphids. Insecticides used for cucumber beetle control should be applied on an as-needed basis rather than at regularly scheduled intervals, especially after transplants have become well-established and vines are growing rapidly.
Insecticides effective against aphids are available, but they should be used only when and where necessary to control critically high population levels. Insecticide application intended to reduce the transmission of virus particles through aphid control usually is not effective. When an infestation is discovered, the grower should look for predators and parasitized aphids. Mark the infestation with flags and return to inspect it in 5 - 7 days. If the beneficial insects are keeping the aphid population in check, no treatment is necessary. If the aphid population is continuing to spread, treatment may be justified. Because aphid infestations often are localized, spot spraying maybe effective.
Two types of cucumber beetles, striped (Figure 69) and spotted (Figure 70), attack watermelons and muskmelons. Cucumber beetle larvae feed on roots and stems and can cause considerable damage (Figure 71), especially if feeding occurs before vines begin to grow vigorously in the spring. The beetles also feed on watermelon and muskmelon rind late in the season, causing cosmetic damage that may reduce market quality. Cucumber beetles are a major concern to muskmelon growers because the insects serve as vectors for the transmission of the bacterial wilt pathogen (see pages 26-27).
Soil-applied systemic insecticide treatment is essential for beetle management in large commercial muskmelon operations. Systemic insecticides will provide 2 - 4 weeks of cucumber beetle control. Repeated applications of contact insecticides are necessary to protect muskmelon plants from beetle feeding and subsequent transmission of the bacteria. There usually will be a massive surge in beetle activity each spring that will last about two weeks. The timing of this surge varies from year to year, and it is the most important time to control the beetles. Applications of foliar insecticides may be required twice per week during peak beetle activity. Monitoring beetle populations through a comprehensive scouting program may be the most effective method to determine when insecticide sprays should be applied. Because watermelons are not susceptible to the wilt disease, protection is necessary only when plants are small and beetle populations are high. Scouting programs may contribute to the most efficient use of insecticides for managing cucumber beetles on watermelon crops.
Mites are arthropod pests that are related to spiders. Damage caused by mites is almost exclusively limited to watermelons, although infestations can be found on muskmelons near the very end of the harvest period. Mites feed on the undersurface of leaves. They suck the sap from the plant and, in hot, dry weather, can defoliate vines in a few weeks. Melons from severely infected plants are often unmarketable because defoliated plants tend to yield small, poor quality fruit.
Mite infestations usually first occur at the edge of a field, frequently next to a gravel road. Colonies establish themselves at the crown of the plant. As populations increase, infested leaves turn yellow and become visible from a distance. Figure 72 shows infested watermelon plants adjacent to a fencerow; the yellow leaves at the crown of the plants are characteristic signs of mite infestation. Close inspection of affected leaves reveals a distinct interveinal yellowing (chlorosis) on the upper surface (Figure 73). The undersides of affected leaves appear tan or yellow and have a crusty texture. Figure 74 shows the underside of a healthy muskmelon leaf and one that is mite infested. Mite-infested plants produce fruit with characteristically coarse surfaces that are readily discernable from the smooth rind of healthy melons. Mites can be identified by shaking symptomatic leaves over a sheet of white paper or by observing infected leaf areas with a 10x hand lens.
Many natural enemies of mites normally inhabit midwestern watermelon fields. They are important regulators of mite populations. Many insecticides used for cucumber beetle control also kill beneficial insects that keep mite populations in check. Therefore, it is best to apply insecticides for cucumber beetle control on an as-needed basis rather than at regularly scheduled intervals, especially after transplants have become well established and vines are growing rapidly.
Miticides are available but should be used only where and when justified by mite population levels. Because mite populations often are localized, spot spraying may be effective.
Seed corn maggots can be responsible for considerable loss of young plants under certain environmental and cultural circumstances. The maggots are larvae of flies that lay eggs into decaying organic matter during the cool, wet weeks of mid-spring. The flies can be attracted to fall-seeded rye cover crops that are plowed down before melon transplanting, or they can be attracted to the commercially prepared soilless growing mix that is used to start the melon seedlings in the greenhouse. Both the plowed down rye and the growing mix represent highly organic material preferred by the adult flies. The maggots are capable of boring into stems of young transplants (Figure 75), causing the seedlings to collapse and die within a few days (Figure 76). Watermelon and muskmelon seedlings are affected by seed corn maggots. Several generations of seed corn maggots can occur if cool, wet weather persists. Warm, dry weather that normally arrives by mid-May reduces the threat of continued maggot damage.
Melons that are transplanted into fields of plowed down rye apparently are at greatest risk of seed corn maggot damage. However, using the cover crop is an advisable field practice and should not be discouraged. Rye should be plowed 3-4 weeks in advance of transplanting to allow sufficient time for green manure to decompose. Maggot control also is necessary in the green house, and especially on wagons used for raising seedlings. Avoiding cool, damp conditions in seedling production facilities may lessen the chance of adult flies laying their eggs in the organic growing mix.
The use of a systemic soil insecticide at planting has only limited effective ness against seed corn maggots.
Discussed below are four disorders of uncertain nature that have been observed in commercial melon fields over the past 10 years. In three of the cases, the cause is unknown. In the fourth case, a presumably pathogenic fungus has been isolated, but conditions surrounding the occurrence and management of the disorder remain in doubt.
Cross stitch is the name given to this disorder by Dr. Don Maynard of the University of Florida. It is characterized by elliptical or oval lesions that tend to be positioned perpendicular to vascular bundles on watermelon rind (Figures 77 and 78). The disorder occurs very infrequently. Cross stitch was observed in Indiana in the late 1980s and early 1990s. Attempts to isolate a pathogenic organism from affected tissue were not successful and confirmed initial suspicions that cross stitch is a non-infectious disorder.
This is an inconspicuous disease whose name also was coined by Don Maynard of the University of Florida. Symptoms are small (1/4 - 3/4 inch) light olive green blemishes on watermelon rind (Figure 79). The blemishes are barely raised (1/8 inch) from the fruit surface and cause a slight discoloration under the skin of the rind (Figure 80). The disorder does not appear to predispose the melons to fruit rot. Attempts to isolate microorganisms associated with the symptoms yielded inconsistent results. Watermelons with greasy spot symptoms were observed rarely during the past decade. Inspection of fields in which affected melons were observed suggested that any yield losses or economic damage attributed to greasy spot were negligible.
This disorder is marked by very striking target-like patterns that occur on the watermelon rind surface. The target spots appear in distinct clusters and can be as large as 1 inch in diameter (Figure 81). The target rings have a corky texture and are slightly raised (1/16 inch) from the fruit surface. No decay was associated with symptomatic fruit. Several attempts at identifying pathogenic bacteria or viruses were not successful. Fruit with the target cluster apparently occur very infrequently. Incidence and distribution in affected fields suggest that it was not responsible for any economic consequences.
Fusarium fruit rot occurs routinely on midwestern muskmelon fruit. However, severe occurrences that result in heavy yield losses are infrequent. Lesions most often appear on the bottom of the fruit, where the melon makes contact with soil. The exterior of affected fruit exhibits a small (1/4 - 3/4 inch) brown or red-purple stain where infections occurred. After the fruit has been cut open, the decay that extends into the melon flesh becomes visible (Figure 82). Al though a species of Fusarium is consistently isolated from symptomatic fruit, the nature of the disease is not well understood. More importantly, manageable factors that contribute to disease development have not been identified.
Greenhouse-grown transplants are relatively new to midwestern melon production. Until recently standard practices involved planting seeds in spent mushroom compost packed into veneer bands in crudely constructed hotbeds. The transformation to modern production practices began within the past 10 years. The veneer bands and compost were replaced with plastic trays and commercially prepared growing mix. Soon after, the hotbeds were abandoned for new greenhouses complete with furnaces and thermostat-controlled exhaust fans. The result was an ample and inexpensive supply of transplants. Although growers generally are more confident in the health and vigor of plants raised under their control, the modern on-site facilities actually increase the vulnerability of the plants to infectious diseases, especially those that are seed-borne such as bacterial fruit blotch, anthracnose, and gummy stem blight. Damping-off also can occur in transplant facilities; however, the Pythium fungus does not represent as great a threat to the entire crop as the seed-borne diseases cited above.
For disease to become established in any situation, three conditions must be satisfied. The pathogen must be present, there must be a susceptible host, and the environment must be conducive for infection and disease spread. In most transplant production facilities, two of those conditions are always present. First, watermelon and muskmelon varieties preferred by midwestern markets are equally susceptible to the common fruit and foliage diseases. As seedlings approach the two-true leaf stage of development, they form a nearly continuous mat of susceptible plant material (Figure 83). Second, the warm humid atmosphere that benefits the development of vigorous transplants also favors the establishment of infectious disease. Once disease is established, the overhead sprinkler irrigation provides an ideal mechanism for spread of bacteria and fungal spores throughout the greenhouse.
Successful management begins with early detection of the problem and accurate diagnosis. Almost all infectious disorders are first discovered when one or several clusters of plants exhibit similar symptoms. Figure 84 shows a cluster of several dozen collapsed seedlings in a pattern that is characteristic of seed-borne infectious disorders. Careful daily inspection of seedlings with special attention given to a clustered distribution of abnormal plants will result in the earliest possible detection if a problem does arise. The melon seedling diseases discussed below may appear indistinguishable to the untrained eye, but the differences between them should become evident after careful inspection.
Bacterial fruit blotch (see pages 26 and 27) is a seed-borne disease that was discovered in 1989 after the appearance of several clusters of symptomatic plants in each of the greenhouses where the pathogen became established. Initial symptoms appear as watersoaked areas on the underside of infected cotyledons (Figure 85). As cotyledons expand, lesions become dark brown and often extend along the length of the midrib (Figure 86). Lesions on young true leaves are small, dark brown, and often are surrounded by a band of yellow tissue (Figure 87). Unlike other fruit and foliage diseases of melons, the fruit blotch-infected seedlings usually do not collapse and die in the greenhouse, but foliar lesions will increase slowly under favorable environ mental conditions.
Bacteria are not wind-dispersed like the spores of many fungal plant pathogens. In the greenhouse, bacteria produced on the surface of a lesion are splashed to adjacent plants during irrigation. Unless the leaf surfaces dry within an hour, the neighboring plants likely will become infected and probably will exhibit symptoms within 4- 10 days. The same method of dispersal is responsible for the spread of fruit blotch in the field.
Like many bacterial pathogens, this pathogen apparently does not overwinter in the absence of host material. Therefore, if greenhouses are properly sanitized, and affected fields are rotated out of host crops, and volunteers are eliminated with appropriate herbicides, the disease is not likely to present major problems in subsequent years unless the pathogen is once again introduced with the seed.
Until 1991, anthracnose never had been reported among melon transplants raised in Indiana. But in the spring of that year, the disease was identified on greenhouse-grown seedlings of a certain watermelon variety. Small, distinct clusters of dead or dying plants (perhaps 25-200 plants) were the first obvious signs of the disease (Figure 88). Sunken stem lesions that are tan or tan pink (Figure 89) will develop quickly and cause the entire seedling to collapse within two weeks of infection. The cotyledons usually wither and die soon after infection. The dark brown lesions that develop on true leaves are roughly oval or circular, small (1/8 - 1/ 4 inch in diameter), and are characterized by sharp or angular margins (Figure 90). Stem lesions produce hundreds of thousands of spores that are splash-dispersed to neighboring plants. New infections become visible to the trained observer within 5-7 days. Once established in the field, anthracnose results in the decline and decay of affected vines and fruit (see pages 24 and 25).
The anthracnose fungus survives in association with infested crop residue and can overwinter in the greenhouse. For any grower who had anthracnose-infected seedlings in a greenhouse or other transplant production structure, the disease presents a very significant threat to the entire crop in the following season. Such growers not only must give special attention to disease prevention in the greenhouse, but also must avoid affected fields for several years.
The gummy stem blight (GSB) pathogen (see pages 38 and 39) probably was introduced with contaminated seed several times within the past 10 years. However, unlike the situations with bacterial fruit blotch and anthracnose, no single variety or seed lot was identified as the source of contamination. As with the other diseases, small clusters of abnormal plants are the first obvious sign of the disease. Figure 91 shows a single tray of seedlings with an obvious cluster of GSB-infected plants. Infection results in a collapse of the cotyledons and brown spots on true leaves, causing some people to confuse GSB with fruit blotch or anthracnose. However, the diagnostic symptom of GSB infection is the presence of a watersoaked lesion at the top of the seedling stem (Figure 91). The lesion becomes tan as it matures, but does not become sunken. Small, black, spore-producing structures develop within the tan stem lesions. In a moist environment, the structures release thousands of spores that may be splash-dispersed to neighboring plants. New lesions will appear within 5-10 days, and seedlings may begin to collapse after two weeks.
The GSB pathogen also will survive in the greenhouse in association with infested plant debris, and therefore represents a threat to subsequent crops, including greenhouse-grown transplants. The greenhouses should be sanitized, and heavily infested fields should be rotated out of susceptible crops for about 3-4 years.
It should be no surprise that the most severe greenhouse epidemics occur when the pathogen is present at the time of seeding, in the form of infested plant residue or contaminated seed. Therefore, preventing the initial establishment of disease in the greenhouse is essential for a healthy crop of transplants. Successful growers do not plant seed saved from their own melons and must rely on the seed industry to distribute uncontaminated seed. Although most seed companies are intensifying their efforts to produce healthy seed, some pathogen-infested seed occasionally reaches the farm. Unfortunately, such seed-borne diseases often result in disastrous losses in the field that may continue to plague the grower for years.
Certain precautions can be taken to eliminate the survival of inoculum in the greenhouse. Greenhouse production surfaces (floors, walls, benches, etc.) should be cleared of any plant residue and treated with a 10% bleach solution. Plastic growing trays that were used to raise infected transplants should not be reused unless they are thoroughly washed and disinfested with the bleach solution. Some weeds can harbor plant pathogens and therefore should not be allowed to grow in or around the greenhouse. Other measures can be taken to create a somewhat less favorable environment for disease development. Irrigation should be scheduled for the morning hours so that plant surfaces will dry as quickly as possible. Also, growers can briefly vent the greenhouse in the evening to release warm, humid air and allow cooler, dryer air into the structure. Heating the cool air by briefly firing the furnace will promote air movement around the plants and keep plant surfaces dry during the night.
It is not likely that any of the recommendations above will completely eliminate infectious disease from the greenhouse. Certainly, if seed is uncontaminated to begin with, epidemics of fruit blotch, anthracnose, and gummy stem blight will occur less frequently and be much less severe. Growers who succeed in keeping their greenhouse-grown transplants healthy will be those who exercise all possible precautions to reduce risk of infectious disease.
For further information contact Richard Latin, Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907-1155.
The author wishes to thank reviewers whose suggestions improved the manuscript, and especially Rick E. Foster, Department of Entomology, Purdue University who contributed to and edited the section on Arthropod Pests.
Cooperative Extension work in Agriculture and Home Economics, state of Indiana, Purdue University, and U.S. Department of Agriculture cooperating; H. A. Wadsworth, Director, West Lafayette, IN. Issued in furtherance of the acts of May 8 and June 30, 1914. The Cooperative Extension Service of Purdue University is an affirmative action/equal opportunity institution.