Part I. Infectious Diseases Diseases of Subterranean Plant Parts Caused by Fungi and Oomycetes Many different fungi, plus bacteria and oomycetes, cause root rot and vine declines on cucurbits. The damage to the roots often leads to secondary symptoms in the aboveground portions of plants. Principal diagnostic characteristics include visible root symptoms, stem gumming, crown lesions, and pathogen fruiting structures (Table 10). In addition to the distinct root and stem rots listed in the following sections, several fungi and a bacterium that cause fruit rots also cause various degrees of root rot. See the sections on bacterial soft rot, crater rot, Lasiodiplodia fruit rot, Phomopsis fruit rot, and red rot in the section on preharvest and postharvest fruit rots later in Part I. Fungi and oomycetes known to infect cucurbits are also listed in the appendix. Readers will note that in both the appendix and the text, alternative names of fungi are identified exclusively as “synonyms,” rather than as specific life cycle states (e.g., “anamorph,” “teleomorph”). This practice reflects the policy for naming fungi issued in 2011 by the International Botanical Congress: namely, that the use of multiple names for the same fungus be abandoned. (Readers interested in learning more about this policy are referred to the 2011 article by Hawksworth [see Selected Reference].) Going forward, accommodating this new policy may mean that the most familiar names of some fungi will change. Changes to the names of fungi, as well as other updates to taxonomy and nomenclature, will be made in the Common Names of Diseases list for cucurbits, which is available on the website of The American Phytopathological Society.
Symptoms A range of root symptoms has been observed in field- collected cucurbit plants showing general symptoms of root rot and vine decline, from which A. vagum was isolated. These symptoms include stubbed-off and necrotic root hairs, brown lesions on the primary root, lesions on the juncture of primary and secondary roots, and a dry, corky root rot (Fig. 21). Occasionally, a slight pink pigmentation and microsclerotia are observed in affected secondary roots (Fig. 22).
Causal Organism Acrocalymma vagum (syn. Rhizopycnis vagum) is an asexually reproducing fungus characterized by large, black pycnidia, which are 200–400 µm in diameter and spherical and have an opening with a long to short papilla. Conidiophores are absent. Conidia are hyaline to brown, smooth, straight, cylindrical to fusiform, and guttulate. Each has one to three septa and measures 18–25 × 4.5–6.0 µm (with a range of 16–28 × 4.0–6.9 µm). Chlamydospores are dark brown to black, thick walled, often blistered, and in short to long chains. Microsclerotia have five to six layers of thick-walled, dark brown cells. Colonies on potato dextrose agar produce dense, cottony, grayish brown mycelia. The colony reverse is dark brown with characteristic reddish to purple coloration. The pycnidia of
Selected Reference Hawksworth, D. L. 2011. A new dawn for the naming of fungi: Impacts of decisions made in Melbourne in July 2011 on the future publication and regulation of fungal names. IMA Fungus 2:155-162.
(Prepared by A. P. Keinath)
Acrocalymma Vine Decline Acrocalymma vagum is a soilborne fungus that has been found associated with cucurbit root rot and vine decline in Guatemala, Honduras, Italy, Spain, and the United States (California, Indiana, and Texas). Melon, watermelon, and Cucur bita spp. hybrids used as grafting rootstocks are susceptible. This fungus has also been reported to infect tomato, and it has been isolated from asymptomatic roots of other plants such as Amaranthus sp., grapevine, Pinus halepensis, rosemary, and sugarcane. 24
Fig. 21. Red discoloration of lateral cucurbit roots, one symptom of Acrocalymma vine decline caused by Acrocalymma vagum (syn. Rhizopycnis vagum). Symptoms can be confused with those of pink root. (Courtesy B. D. Bruton–© APS)
25
Porta-P uglia, A., Pucci, N., Di Giambattista, G., and Intantino, A. 2001. First report of Rhizopycnis vagum associated with tomato roots in Italy. Plant Dis. 85:1210. Trakunyingchaoren, T., Lombard, L., Groenewald, J. Z., Cheewangkoon, R., Toanun, C., Alfenas, A. C., and Crous, P. W. 2014. Mycoparasitic species of Sphaerellopsis, and allied lichenicolous and other genera. IMA Fungus 5:391-414. Westphal, A., Xing, L., and Goodwin, S. B. 2011. Mature watermelon vine decline: Suppression with fumigants of a soil-borne problem and association with Rhizopycnis vagum. Crop Prot. 30:111-117.
(Prepared by J. Armengol)
Black Root Rot Fig. 22. Microsclerotia of Acrocalymma vagum in a cucurbit root affected by Acrocalymma vine decline. (Courtesy B. D. Bruton–© APS)
A. vagum are observed rarely on roots of field-grown plants, but they can develop abundantly in cultures grown on water agar with the addition of sterilized fragments of healthy cucurbit roots that are incubated at 20–22°C with 12-h periods of fluorescent light and darkness.
Disease Cycle and Epidemiology A. vagum has frequently been found associated with other soilborne pathogens involved in root rot and vine decline diseases of cucurbits, such as Monosporascus cannonballus and Plectosphaerella melonis (syn. Acremonium cucurbitacearum) (see sections later in Part I). Isolation of A. vagum from affected roots is difficult, because the fungus grows slowly and is overrun by saprophytes on agar. Consequently, it is not easy to determine the frequency of field infections caused by this fungus or to establish its role as a pathogen of cucurbits. In general, it is considered a weak pathogen and a contributor to root rot and vine decline through infection of roots. The presence of A. vagum on roots of very diverse plant species suggests that weeds and other crops may affect its survival or increase its inoculum potential in soil. In addition, microsclerotia and chlamydospores can play an important role in the epidemiology of the fungus as overseasoning inoculum sources.
Management
Black root rot is an occasional disease of watermelon caused by Thielaviopsis basicola. This disease is typically observed in greenhouses, and it has not been known to cause losses in fields in the United States, with the exception of one recent case in the Southeast.
Symptoms Black root rot symptoms in watermelon are similar to those caused by many root diseases in cucurbits. These symptoms include chlorosis of the foliage, lack of vigorous growth, and stunting, wilting, or collapse of the entire plant. Belowground symptoms are dark brown to black lesions that occur primarily on root tips and may run lengthwise along the roots. The black root tips resemble damage caused by the sting nematode (Belo nolaimus longicaudatus). Roots deteriorate and cease to function. Diseased plants appear stunted compared with healthy plants but may remain alive for some time (Fig. 23). Black root rot is more commonly found in greenhouse transplants than in the field. Symptoms on young plants resemble those of other diseases, such as root rots caused by Pythium or Fusarium spp. or Rhizoctonia solani.
Causal Organism The causal agent of black root rot of watermelon is Thielavi opsis basicola. This soilborne fungus attacks more than 137 plant species in 33 families. It is a hemibiotrophic pathogen that requires living host cells for infection to occur but also has phases of necrotrophic behavior, killing host cells and sporulating on dead tissue. There is no known sexual state.
Long-term crop rotations may be required for adequate management of A. vagum because of the presence of its resistant microsclerotia and chlamydospores in soil after continuous cucurbit cultivation. Other cultural management strategies recommended against cucurbit root rot and vine declines, such as drip irrigation or grafting onto hybrid rootstocks of Cucurbita spp., can be useful to manage A. vagum. Recent research indicates that the pathogen can be managed by soil fumigation or a heat treatment of soil at or above 60°C for 30 min. Selected References Aegerter, B. J., Gordon, T. R., and Davis, R. M. 2000. Occurrence and pathogenicity of fungi associated with melon root rot and vine decline in California. Plant Dis. 84:224-230. Armengol, J., Vicent, A., Martínez-Culebras, P., Bruton, B. D., and García-Jiménez, J. 2003. Identification, occurrence and pathogenicity of Rhizopycnis vagum on muskmelon in Spain. Plant Pathol. 52:68-73. Chilosi, G., Reda, R., Aleandri, M. P., Carmele, I., Altieri, L., Montuschi, C., Languasco, L., Rossi, V., Agosteo, G. E., Macrì, C., Carlucci, A., Lops, F., Mucci, M., Raimondo, M. L., and Frisullo, S. 2008. Fungi associated with root rot and collapse of melon in Italy. EPPO Bull. 38:147-154. Farr, D. F., Miller, M. E., and Bruton, B. D. 1998. Rhizopycnis vagum gen. et sp. nov., a new coelomycetous fungus from roots of melons and sugarcane. Mycologia 90:290-296.
26
Fig. 23. Stunted and wilted seedless watermelon plants infected with Thielaviopsis basicola, causal organism of black root rot, on either side of unaffected pollenizer plants that originated from a different seedling tray. (Courtesy E. D. Beasley–© APS)
Fig. 24. Chlamydospores of Thielaviopsis basicola. (Courtesy G. S. Abawi. Reproduced, by permission, from Compendium of Bean Diseases, 2nd ed., 2005, American Phytopathological Society, St. Paul, MN)
Disease Cycle and Epidemiology Chlamydospores (Fig. 24) and endoconidia are the primary inocula that are spread easily in soil, media, or contaminated peat moss. Chlamydospores can survive on reused transplant trays or other greenhouse implements used for planting. Once roots of watermelon transplants are infected, the fungus proliferates on decaying root tissue, producing numerous chlamydospores along the root surface as well as within root tissue. Occasionally, infected transplants are asymptomatic in the field until heat or water stress occurs. Symptoms observed in the field appear as a gradual wilt, developing at the peak temperature of the day. Wilting becomes more advanced and permanent as the disease progresses.
Management Fungicides used as soil or plant drenches have worked as protectants against T. basicola. Management that is more effective includes the application of soil fumigants, sanitation of greenhouse trays, use of healthy transplants, and crop rotation. Crop rotations should avoid plants known to be susceptible to T. basicola in a given production region, such as beans, carrot, cotton, soybean, or tobacco. Since the pathogen is sensitive to acidic soil conditions, it is also recommended that soil pH be kept near 6.0 in infested fields. Research has shown that excess liming can promote pathogen activity. Selected References Koike, S. T., and Henderson, D. M. 1998. Black root rot, caused by Thielaviopsis basicola, on tomato transplants in California. Plant Dis. 82:447. Meyer, J. K., and Shew, H. D. 1991. Soils suppressive to black root rot of burley tobacco, caused by Thielaviopsis basicola. Phytopathology 81:946-954. Mims, C. W., Copes, W. E., and Richardson, E. A. 2000. Ultrastructure of the penetration and infection of pansy roots by Thielaviopsis basicola. Phytopathology 90:843-850.
(Prepared by E. D. Beasley and D. B. Langston, Jr.)
Charcoal Rot Macrophomina phaseolina is one of several fungi that cause vine decline in cucurbits (Table 10). Although thought to be of relatively minor importance, it can be severe in cantaloupe and honeydew under certain environmental conditions. It has occa-
Fig. 25. Vine lesion of charcoal rot on melon caused by Macro phomina phaseolina. (Courtesy B. D. Bruton)
sionally been observed in watermelon, cucumber, and squash. The disease has been observed in practically all cucurbit- growing areas of the world.
Symptoms Symptoms in melon include yellowing and death of crown leaves and a water-soaked lesion that encompasses the vine at the crown. These symptoms normally begin to appear just prior to harvest. The lesion may extend 5–15 cm up the vine (Fig. 25). Characteristic droplets of amber exudate (gumming) are produced in the affected area and eventually dry to a dark brown. The water-soaked charcoal rot lesion appears dry and tan within a few days, accompanied by numerous stem cracks, giving it a “weathered stump” appearance. Small, black microsclerotia are typically embedded in the diseased tissue. Under humid or wet conditions, they may be accompanied by pycnidia. The disease at this point looks almost identical to gummy stem blight. However, a gummy stem blight lesion typically has numerous pycnidia and pseudothecia embedded in its older parts (see the section Gummy Stem Blight later in Part I). Stunting and reduced root growth have been observed in melon plants infected with M. phaseolina, but root rot is observed only in the latter stage of disease development. Cross sections of the affected area reveal necrotic epidermal cells and a few necrotic subepidermal cells. As the disease progresses, the fungus penetrates the area between the vascular bundles. It subsequently colonizes the vascular bundles, causing death of the plant. The time from the appearance of the first symptom to the death of the vine varies from about 10 to 20 days. Occasionally, the fungus penetrates a few (three to five) vascular bundles early in disease development. The discolored vascular bundles can be traced up the stem, and the portion of the leaf that is fed by them dies. This symptom may resemble symptoms of Fusarium wilt; however, wilting and a general yellowing of all the leaves is characteristic primarily of Fusarium wilt, while leaf yellowing and necrosis are restricted mainly to the crown leaves in charcoal rot (see the section Fusarium Wilt of Melon later in Part I). Because of the loss of crown leaves, sunburn may occur, resulting in unmarketable melons. Symptoms of charcoal rot in watermelon are not as intense as those in melons. Crown lesions tend to be more restricted, developing a reddish brown appearance without the associated gumming observed in melon. Microsclerotia develop in the lesion. The disease rarely causes detectable damage to watermelon. All cucurbit fruit are susceptible to charcoal rot, although it occurs more frequently in cucumber and melon and occasionally 27
in honeydew (Fig. 26). Watermelon is rarely affected, probably because of its thick wax coating and epidermis. Pumpkins are occasionally infected. Injury likely plays a major role in fruit infection. A cross section of infected fruit reveals a firm decay, with the color changing from normal to pink or wine red to black in the oldest part of the lesion (Fig. 27). The black color results from development of microsclerotia. Not all isolates produce the reddish pigment in the fruit.
Causal Organism Macrophomina phaseolina causes charcoal rot. Because sexual reproductive structures have not been observed, M. phaseolina apparently exists only as vegetative mycelium, microsclerotia, and pycnidia. Considerable variation in virulence, pigment biosynthesis, and pycnidial production exists within the species. Young hyphae are hyaline and darken with age. Microsclerotia vary in shape, from spherical to oblong, oval, elliptical, or even forked, and vary in length from 25 to 150 µm. Microsclerotia from laboratory cultures range from 50 to 200 µm in diameter. Pycnidia, with diameters of 100–200 µm, are black, roughly spherical structures and may closely resemble microsclerotia in size, shape, and color. Pycnidia are almost totally embedded in the host tissue. The single-celled conidia are hyaline and ellipsoidal or ovoid, mea-
suring 14–30 × 5–10 µm. The conidia germinate readily and are infectious.
Disease Cycle and Epidemiology Microsclerotia in the soil and plant debris usually serve as primary inoculum, and the pathogen can be seedborne. Infection seems to occur almost exclusively on secondary and tertiary roots. Extensive colonization of the root system can occur without noticeable discoloration until microsclerotia begin to form. Root rot caused by M. phaseolina in cucurbits tends to coincide with vine senescence. Secondary inoculum is produced by the pycnidial phase under warm and wet conditions; nevertheless, aerial infection of plant parts has been rarely documented. A high percentage of melon root systems may become infected by 49 days after planting in infested fields. The fungus is present in the crown soon after infection of the root system, although disease symptoms normally do not develop until about 75–85 days after seeding. In a similar fashion, M. phaseolina is a latent pathogen on melon fruit. Drought stress and high temperature are not required for infection of melon roots, although they have been reported to be required for infection of roots of other cucurbit hosts by other pathogens. Drought stress and high temperature are likely important for disease development, however.
Management Little success has been achieved with soil fumigants in managing charcoal rot in cucurbits, and their effectiveness is highly dependent on soil type. Solarization has not been effective, and little or no benefit can be realized by maintaining adequate soil moisture. Deep plowing is of little value, because of the vertical distribution of the fungus and the fact that even one colony- forming unit per gram of soil can cause infection. Because of the extremely wide host range of the pathogen, crop rotation is not practical. Grafting melons onto Cucurbita spp. rootstocks along with fungicide application has shown some promise. Biological control with various Pseudomonas and Trichoderma spp. has also shown some promise. Some melon and honeydew hybrids show a high level of resistance to the vine-decline phase, whereas others are highly susceptible. In general, honeydews tend to be more resistant than melons. Evidence suggests that resistance to M. phaseo lina is not simply inherited. Fig. 26. External symptoms of charcoal rot on melon, caused by Macrophomina phaseolina. (Courtesy G. J. Holmes–© APS)
Fig. 27. Charcoal rot symptoms in melon fruit flesh, caused by Macrophomina phaseolina. (Courtesy B. D. Bruton–© APS)
28
Selected References Bruton, B. D., and Reuveni, R. 1985. Vertical distribution of microsclerotia of Macrophomina phaseolina under various soil types and host crops. Agric. Ecosyst. Environ. 12:165-169. Bruton, B. D., Jeger, M. J., and Reuveni, R. 1987. Macrophomina phaseolina infection and vine decline in cantaloupe in relation to planting date, soil environment, and plant maturation. Plant Dis. 71:259-263. Cohen, R., Oman, N., Porat, A., and Edelstein, M. 2012. Management of Macrophomina wilt in melons using grafting or fungicide soil application: Pathological, horticultural and economical aspects. Crop Prot. 35:58-63. Dunlap, J. R., and Bruton, B. D. 1986. Pigment biosynthesis by Macro phomina phaseolina: The glycine-specific requirement. Trans. Br. Mycol. Soc. 86:111-115. Mihail, J. D., and Alcorn, S. M. 1984. Effects of soil solarization on Macrophomina phaseolina and Sclerotium rolfsii. Plant Dis. 68:156-159. Oosthuizen, M. M. J., and Potgieter, D. J. J. 1974. Induction of photosporogenesis in Macrophomina phaseoli by octadecenoic acid from peanuts. Phytochemistry 13:1027-1029. Reuveni, R., Krikum, J., Machimias, A., and Shelvin, E. 1982. The role of Macrophomina phaseolina in a collapse of melon plants in Israel. Phytoparasitica 10:51-56.
(Prepared by B. D. Bruton and C. L. Biles)
Fusarium Crown, Foot, and Fruit Rot Fusarium crown, foot, and fruit rot of cucurbits was first described in detail in 1932 from South Africa. The disease occurs in many countries around the world, and most cucurbits are susceptible, including melons and cucumber; however, Cucur bita spp., especially C. pepo (pumpkins and squash) appear to be particularly susceptible and often sustain significant losses. The disease has been described by various names, including wilt, root and stem rot, fruit rot, and cortical rot.
later in Part I). F. solani f. sp. cucurbitae is a member of the Fusarium solani species complex (FSSC), containing perhaps 45–50 related but phylogenetically distinct species distributed among three major clades. Because of the high morphological similarity of the asexual and sexual states within the complex, the Latin Fusarium and Nectria binomials have not been proposed for most of the biological species within this group. Instead, these species are generally identified broadly as F. solani and by their N. haematococca mating population (MP) designations, MP I through MP VII. Formerly, the two “races” of F. solani f. sp. cucurbitae were referred to in the plant pathology literature as Fsc-1 and Fsc-2. These races
Symptoms Plants of all ages are susceptible to infection, and young seedlings may experience high levels of pre-and postemergence damping-off. Usually, the first symptom noticed in the field is a yellowing and wilting of the leaves as a result of the root rot stage. In severe cases, the entire root may rot, resulting in death of the plant. The rot develops first as a light-colored, water-soaked area, which becomes progressively darker. It begins in the cortex tissue of the root, causes the cortex to slough off, and eventually destroys most of the root tissue, except the fibrous vascular strands (Fig. 28). Infected plants break off easily at or near the soil line. The fungus is generally limited to the crown area of the plant and upper taproot. Plants showing symptoms develop numerous sporodochia and macroconidia, giving the mycelia a white to pink color that typically darkens with age. Fruit also can become infected, especially fruit that are bruised or wounded and in contact with the soil. Fruit rot symptoms can vary considerably depending on moisture levels, but most fruit rots begin as small, pitted spots and may progress to larger sunken lesions that may extend into the flesh (Figs. 29–31).
Fig. 29. Fusarium fruit rot of pumpkin caused by Fusarium solani f. sp. cucurbitae. (Courtesy M. Babadoost–© APS)
Causal Organisms The primary causal agent of Fusarium crown, foot, and fruit rot of cucurbits is Fusarium solani f. sp. cucurbitae (syn. Nec tria haematococca), although numerous other Fusarium spp. can cause fruit rots in cucurbits (see the section Fusarium Rot
Fig. 30. Fusarium fruit rot of cucumber caused by Fusarium solani f. sp. cucurbitae. (Courtesy M. Babadoost–© APS)
Fig. 28. Fusarium crown and root rot of watermelon caused by Fusarium solani f. sp. cucurbitae. (Courtesy R. D. Martyn)
Fig. 31. Fusarium fruit rot of melon caused by Fusarium solani f. sp. cucurbitae. (Courtesy M. Babadoost–© APS)
29
are actually phylogenetically distinct species in two different mating populations. F. solani f. sp. cucurbitae race 1 (Fsc-1) is in MP I and causes a cortical stem, root, and fruit rot of most cucurbits. F. solani f. sp. cucurbitae race 2 (Fsc-2), recently renamed F. petroliphilum, is in MP V and attacks only the fruit. F. solani f. sp. cucurbitae occurs throughout much of the cucurbit-growing area of the world, while F. petroliphilum appears to be more limited. Although F. solani f. sp. cucurbi tae and F. petroliphilum are indistinguishable morphologically, they can be differentiated by a PCR protocol in which taxon- specific primers designed from the translation elongation factor 1-α sequences are used or by random amplification of polymorphic DNA markers. In addition to causing plant diseases, phylogenetically distinct members of the species complex are responsible for approximately two-thirds of all fusarioses of humans and other animals. Clade 3 within the complex contains most of the medically important species examined, including isolates that cause sight-threatening fungal corneal infections in contact lens wearers. Within clade 3, there are approximately 36 phylogenetic species of the complex spread among four major groups (lineages). Group 1 (FSSC 1) contains isolates that are members of MP V, including F. petroliphilum, and cause both human and plant diseases. In addition, all isolates within FSSC 1, whether obtained from plants or from human clinical studies, are pathogenic to cucurbits and sexually compatible with cucurbit isolates. Furthermore, all of the FSSC 1 isolates examined thus far grow and sporulate at 37°C, indicating that they are tolerant of the human body temperature, raising important questions about species that may be capable of causing both plant and human diseases.
Disease Cycle and Epidemiology Like many Fusarium spp., F. solani f. sp. cucurbitae and F. petroliphilum survive in the soil as chlamydospores, although reportedly for only 2–3 years. Since ascopores are seldom, if ever, observed in nature, their role in survival is unknown. Both F. solani f. sp. cucurbitae and F. petroliphilum can be seedborne, aiding in the dissemination of the pathogen but with apparent minimal effect on seed germination. Seed can become infested via lesions and wounds in the fruit, although the lesion must extend near or into the flesh. Hyphae of F. solani f. sp. cucurbitae can penetrate the fruit epidermis directly and grow inter-and intracellularly. Sporodochia form readily above the soil line in or near lesions. In contrast, conidia of F. petroliphilum germinate and can grow on the epidermal surfaces of seedling hypocotyls but do not appear to penetrate. Nevertheless, F. petroliphilum readily enters through wounds in the fruit where it causes lesions and rot. Almost all cucurbits tested are susceptible, although there are reports of varying degrees of susceptibility among species. In the field, Cucurbita spp. appear the most affected. High moisture levels in the soil exacerbate the rot symptoms.
Fusarium wilts and other soilborne diseases. Two commonly used rootstocks are C. maxima and C. moschata, but since both are susceptible to F. solani f. sp. cucurbitae, the presence of this pathogen in a field potentially could render the practice of grafted watermelons much less effective. Selected References Armengol, J., José, C. M., Moya, M. J., Sales, R., Vicent, A., and García-Jiménez, J. 2000. Fusarium solani f. sp. cucurbitae race 1, a potential pathogen of grafted watermelon production in Spain. EPPO Bull. 30:179-183. Mehl, H. L., and Epstein, L. 2007. Identification of Fusarium solani f. sp. cucurbitae race 1 and race 2 with PCR and production of disease-free pumpkin seeds. Plant Dis. 91:1288-1292. Mehl, H. L., and Epstein, L. 2007. Fusarium solani species complex isolates conspecific with Fusarium solani f. sp. cucurbitae race 2 from naturally infected human and plant tissue and environmental sources are equally virulent on plants, grow at 37°C and are in fertile. Environ. Microbiol. 9:2189-2199. O’Donnell, K. 2000. Molecular phylogeny of the Nectria haematococca- Fusarium solani species complex. Mycologia 92:919-938. Samac, D. A., and Leong, S. A. 1988. Disease development in Cucur bita maxima (squash) infected with Fusarium solani f. sp. cucurbi tae. Can. J. Bot. 67:3486-3489. Zhang, N., O’Donnell, K., Sutton, D. A., Nalim, F. A., Summerbell, R. C., Padhye, A. A., and Geiser, D. M. 2006. Members of the Fu sarium solani species complex that cause infections in both humans and plants are common in the environment. J. Clin. Microbiol. 44:2186-2190.
(Prepared by R. D. Martyn)
Fusarium Root and Stem Rot Root and stem rot is a disease of cucurbits that was recorded for the first time in Greece on cucumber in 1989 and on melon in 2001 in greenhouse crops. It has subsequently been found in greenhouse cucumber crops in Bulgaria, France, Poland, Spain, Egypt, Iran, Israel, Sri Lanka, China, Turkey, Canada, and
Management A source of good resistance to F. solani f. sp. cucurbitae and F. petroliphilum has yet to be identified; thus, other means of management are necessary. Since the pathogens presumably survive only for a few years in the soil, rotation with noncucurbit plants is a possibility. Because the pathogens also may be seedborne, a visual inspection of fruit should be made before harvesting, and only fruit that are lesion free or have only superficial lesions should be harvested for seed. Fungicide- treated seed should be used when possible. In greenhouse studies, several commercial biocontrol products consisting of bacteria (Pseudomonas spp.) or fungi (Trichoderma spp.) were effective in reducing disease in zucchini (C. pepo) caused by F. solani f. sp. cucurbitae. Grafting watermelon and melons onto Cucurbita spp. rootstock is increasingly becoming more important in managing 30
Fig. 32. Fusarium stem rot of the collar and the lower part of the stem of a young cucumber plant, caused by Fusarium oxysporum f. sp. radicis-cucumerinum. (Courtesy D. J. Vakalounakis–© APS)
Fig. 33. Wilt and chlorosis of an adult cucumber plant affected by Fusarium root and stem rot, caused by Fusarium oxyspo rum f. sp. radicis-cucumerinum. (Cour tesy D. J. Vakalounakis–© APS)
Fig. 34. A unilateral cortical rot with a longitudinal canker at the lower part of the stem of a cucumber plant (right) affected by Fusarium root and stem rot, caused by Fusarium oxysporum f. sp. radicis-cucumerinum. (Cour tesy D. J. Vakalounakis–© APS)
Fig. 35. Vascular discoloration in longitudinal and cross sections of the stem of an adult cucumber plant affected by Fusarium root and stem rot, caused by Fusarium oxysporum f. sp. radicis-cucumerinum. (Courtesy D. J. Vakalounakis–© APS)
Australia. No fruit symptoms have been observed, but wilting and death of the plants result in severe yield losses. The disease has not been reported as a problem in field-grown cucurbits.
Symptoms Symptoms first appear on plants about 1 month old. A collar rot develops, usually on one side of the stem, that ranges from very light green to amber and brown. Progressively the rot becomes more severe, and a white to pink fungal growth may appear on the affected tissue (Fig. 32). The primary root and several secondary roots rot, and the basal portion of the stem shows a vascular light brown discoloration. The growth of plants with these symptoms is stunted, and they wilt and die within a few weeks. Plants can also wilt suddenly and die without developing collar rot. Although young plants can be killed, usually plants reach mature size and symptoms do not appear until the fruit-bearing stage. Adult plants then undergo slow wilting with a progressive yellowing (Fig. 33). Infected plants with heavy fruit loads wilt on sunny days but may recover at night. However, the plants die after repeated wilting. These symptoms usually involve a unilateral cortical rot with a longitudinal canker at the lower part of the stem that may extend upward for about 20–40 cm (Fig. 34) and downward to the root system. In the stem, a vascular yellow to light brown discoloration may appear, extending for 40–200 cm above the soil line (Fig. 35). Primary, secondary, and tertiary roots have brown lesions, many confluent with hypocotyl lesions. Isolated unilateral cracks with rot varying in length from 5 to 15 cm or more, usually with whitish pink growth of the pathogen, might also appear on the upper portion of the stem. Sometimes, a rot with a white to pink fungal growth may also appear farther up on the stem, resulting from direct infection by the pathogen via wound sites from pruning and other mechanical damage (Fig. 36).
Causal Organism The fungus Fusarium oxysporum f. sp. radicis-cucumerinum is the cause of root and stem rot of cucumber and melon. This
Fig. 36. Fusarium stem rot with a white to pink fungal growth of Fusarium oxysporum f. sp. radicis-cucumerinum on the upper part of the stem of a mature cucumber plant. (Courtesy D. J. Vakalounakis–© APS)
pathogen causes primarily a root and stem rot of greenhouse cucumbers, as opposed to a true vascular wilt caused by F. oxy sporum f. sp. cucumerinum (see the section Fusarium Wilt of Cucumber later in Part I). Following artificial inoculation, the fungus also can infect sponge gourd (Luffa aegyptiaca). The pathogen is usually readily isolated from symptomatic vascular tissue. Semiselective media, such as Komada’s medium, 31
can help to isolate the pathogen if secondary organisms are present.
Disease Cycle and Epidemiology F. oxysporum f. sp. radicis-cucumerinum survives on plant debris and other organic matter in soil as chlamydospores for at least 13 months. It can be locally disseminated by infected transplants and in windborne and waterborne contaminated soil. Fungus gnat adults appear to aid in the local dissemination of the pathogen. Long-distance spread is through organic substrates and transplants. Seed infection is suspected but has not yet been demonstrated. However, seed infection has been reported for F. oxysporum f. sp. radicis-lycopersici, a similar pathogen of tomato. The pathogen invades through the root tips, wounds that occur during transplanting and nematode attack, and ruptures caused by growth of new lateral roots. The pathogen can also invade the upper portion of the stem through pruning wounds and other mechanical damage. During the winter, when plant vigor within greenhouses is reduced because of unfavorable microclimatic conditions, the disease may progress rapidly, causing severe damage. Disease severity is increased by stress caused by low temperatures and high yield. The optimal temperatures for symptom development are 17–19°C, in contrast to Fusarium wilt (caused by F. oxysporum f. sp. cucumerinum), which is favored by higher temperatures of 27–29°C. For this reason, root and stem rot affects mainly early crops and plants in the coldest spots within greenhouses. In some areas, the disease may appear in early summer and cause severe damage, resulting from highly virulent isolates and high soil moisture levels or great fluctuations between day and night temperatures.
Management Currently, there are no effective curative treatments for root and stem rot. Infected plants should be removed quickly from the greenhouse to prevent spread of the disease. The most effective means of disease management prior to infection is grafting cucumbers onto resistant rootstocks, mainly Cucurbita maxima × C. moschata F1 and C. ficifolia. Other means of disease management include 1) removal and burning of plant residues when the crop season is over; 2) use of disinfested equipment; 3) incorporation of suppressive crop residues (e.g., lettuce) into soil prior to cultivation, with or without soil solarization; 4) heating infested soil or fumigating it with broad-spectrum biocides, although it may be reinvaded; and 5) use of clean, pathogen-free seeds and transplants Soil solarization, especially with the use of virtually impermeable films that greatly reduce the loss of produced biogases, could have some efficacy in managing the disease in greenhouse beds with low inoculum potential. A few tolerant commercial cultivars are available. Selected References Martyn, R. D., and Vakalounakis, D. J. 2012. Fusarium wilt of greenhouse cucurbits: Melon, watermelon, and cucumber. Pages 159-174 in: Fusarium Wilts of Greenhouse Vegetable and Ornamental Crops. M. Lodovica Gullino, J. Katan, and A. Garibaldi, eds. American Phytopathological Society, St. Paul, MN. Pavlou, G. C., and Vakalounakis, D. J. 2005. Biological control of root and stem rot of greenhouse cucumber, caused by Fusarium oxy sporum f. sp. radicis-cucumerinum, by lettuce soil amendment. Crop Prot. 24:135-140. Pavlou, G. C., Vakalounakis, D. J., and Ligoxigakis, E. K. 2002. Control of root and stem rot of cucumber, caused by Fusarium oxysporum f. sp. radicis-cucumerinum, by grafting onto resistant rootstocks. Plant Dis. 86:379-382. Vakalounakis, D. J. 1996. Root and stem rot of cucumber caused by Fusarium oxysporum f. sp. radicis-cucumerinum f. sp. nov. Plant Dis. 80:313-316.
32
Vakalounakis, D. J., and Fragkiadakis, G. 1999. Genetic diversity of Fusarium oxysporum isolates from cucumber: Differentiation by pathogenicity, vegetative compatibility, and RAPD fingerprinting. Phytopathology 89:161-168. Vakalounakis, D. J., Doulis, A., and Klironomou, E. 2005. Virulence of Fusarium oxysporum f. sp. radicis-cucumerinum to melon under natural conditions. Plant Pathol. 54:339-346.
(Prepared by D. J. Vakalounakis and R. D. Martyn)
Fusarium Wilts Cucurbits are affected by at least seven vascular wilt diseases caused by different formae speciales (“special forms”) of Fu sarium oxysporum that are morphologically similar but generally host specific (Table 11). In addition, several races have been described within different formae speciales. No sexual reproductive state of F. oxysporum is known; however, the asexual state has several spore forms. Microconidia (Fig. 37) are abundant, oval to kidney shaped, formed on short monophialides (simple conidiophores), and generally one celled, although two-celled microconidia occur. Macroconidia (Fig. 38) are fusiform, have three to five cells, and are produced in large numbers, often in sporodochia; each has a pronounced apical cell and foot-shaped basal cell. Chlamydospores (Fig. 39) are formed from macroconidia and within the mycelia. Chlamydospores formed in mycelia tend to occur singly or in pairs and may be either intercalary or terminal. On potato dextrose agar, F. oxysporum grows rapidly and typically produces white, fluffy, aerial mycelium. Pigmentation in the medium is variable but is often light to dark purple. There is considerable genetic diversity within F. oxysporum, and numerous techniques have been employed to examine relatedness between isolates within and among different formae speciales. Thus far, no single technique or combination of techniques completely answers the relatedness question. Vegetative compatibility groups (VCGs) may be the most practical technique, because pathogenic subgroups often are limited to one or a few VCGs and isolates within a VCG tend to be more similar than isolates in different VCGs (Table 11). There are exceptions to this generality, however; and other phenotypic, genetic, and nuclear markers should be used in conjunction with vegetative compatibility. Fusarium wilts are characterized by wilting of the host, which is induced by several mechanisms, including a breakdown and blockage of xylem elements, formation of tyloses, and alteration of the plant’s water potential and subsequent reduction in water transport through the pit membranes. The cucurbits discussed in the following sections are cucumber, gourds, melon, and watermelon. Fusarium wilt is an economically important disease of each of these crops. No forma specialis of F. oxysporum specific to squash (Cucurbita pepo) has been described; however, some cultivars of summer squash are susceptible to certain isolates of F. oxysporum f. sp. niveum, which causes Fusarium wilt of watermelon. Cucurbit-infecting formae speciales of F. oxysporum may cross infect cucurbits that are not their specific hosts; but in these cases, severe disease symptoms rarely appear, except in seedlings and young plants. In general, cross infection by the cucurbit wilt fusaria is a laboratory and greenhouse phenomenon. In the field, the cucurbit wilt fusaria rarely cross infect and cause wilt. In terms of their disease cycles, epidemiology, and management, the Fusarium wilts of cucurbits are similar. The vascular wilt fusaria are cosmopolitan, occurring throughout the cucurbit-growing regions of the world. Each pathogen is soilborne, long lived, and persistent in the soil and can be seed transmitted. Vascular wilt fusaria can attack their hosts at any