|Crop Knowledge Master||Fungi|
|blight, black leafspot, gray leafspot (Plant Disease Pathogen)|
Stephen A. Ferreira, Extension Plant Pathologist
Rebecca A. Boley, Educational Specialist
Department of Plant Pathology,CTAHR
University of Hawaii at Manoa
These pathogens affect most cruciferous crops, including broccoli and cauliflower (Brassica oleracea L. var. botrytis L.), field mustard and turnip (B. rapa L. (synonym: B. campestris L.), leaf or Chinese mustard (B. juncea), Chinese or celery cabbage (B. pekinensis), cabbage (B. oleracea var. capitata), rape (B. campestris), and radish (Raphanus sativus).
A. brassicae and A. brassicicola are cosmopolitan in their distribution but occur sporadically. A. raphani is widespread in the Northern hemisphere. The pathogens are greatly influenced by weather with the highest disease incidence reported in mild, wet seasons and in areas with relatively high rainfall (Humpherson-Jones and Phelps, 1989).
A. brassicae and A. brassicicola can affect host species at all stages of growth, including seeds. On seedlings symptoms include dark stem lesions immediately after germination, that can result in damping-off, or stunted seedlings. A. raphani produces black stripes or dark brown, sharp-edged lesions on the hypocotyl of the seedling. It grows in the vascular system and rapidly infects the entire seedling (Valkonen and Koponen, 1990). When older plants become infected, Alternaria symptoms often occur on the older leaves, since they are closer to the soil and are more readily infected as a consequence of rain splash or wind blown rain. Late infection, or infection of older leaves, does not characteristically reduce yiedls, and can be controlled through intensive removal of infected leaves (Chupp and Sherf, 1960). Fruit-bearing branches and seed pods show dark or blackened spots that result in yield loss due to premature pod ripening and shedding of the seeds. Infection can also occur on the fruit, before or after harvest. A common symptom of broccoli and cauliflower infection is a browning that occurs on the head.
All three pathogens are destructive diseases for seed growers. The pathogens can shrivel seeds within the pods or kill the pod stalks before seed formation. They may also be a means by which bacterial soft rot enters the stem, which may lead to plant death. (Chupp and Sherf, 1960). In addition to destruction of a seed crop, the pathogens can live within the seed, spread the disease to other fields, and cause a loss of seedlings (Rangel, 1945).
Conidiophores of A. brassicae produce asexual spores (conidia) that measure between 160-200 Ám long. Sporulation occurs (in vitro) between the temperatures of 8 to 24 C where mature spores occur after 24 to 14 hours, respectively. Optimum temperatures are between 16 and 24 C where sporulation time ranges from 12 to 14 hours. A. brassicicola sporulates in a temperature range of 8 to 30 C, where mature spores occur after 43 and 14 hours respectively. Optimum temperatures are between 18 and 30 C where the average sporulation time is 13 hours. Moisture in the presence of rain, dew, or high humidity is essential for infection, and a minimum of 9-18 hours is required for both species (Humperson-Jones and Phelps, 1989). Continuous moisture of 24 hours or longer practically guarantees infection (Chupp and Sherf, 1960; Rangel, 1945). Relative humidity of 91.5% (at 20 C) or higher will result in the production of large numbers of mature spores in 24 hours (Humpherson-Jones and Phelps, 1989).
A. brassicae germinates (in vitro) over a wide range of temperature, 8 C to 31 C, but occurs most quickly, within 3 hours, when the temperature is between 21 and 28 C (at which time 98% of the spores have germinated). As the temperature decreases, the amount of time it takes for 98% of the spores to germinate increases (Degenhardt et al., 1982). A. raphani and A. brassicicola germinate (in vitro) at higher temperatures (tested at a temperature range of 7 to 31 C). The optimum temperatures for A. raphani is 23 C or greater, where after 6 hours of incubation, 98% of the spores germinate. The lowest temperature where 98% of the spores germinate is at 13 C which requires 10 hours of incubation. A. brassicicola begins to germinate 98% of its spores at 15 C after 10 hours of incubation. Ninety-eight percent germination occurs after 3 hours at 31 C (Degenhardt et al., 1982). Plants wound inoculated with A. brassicicola develop symptoms most quickly at 25 C, while seedlings from infected seeds develop symptoms most quickly at 30 C. No germination occurs at 35 C for all three pathogens (Bassey and Gabrielson, 1983). Free water or high humidity is required for germination and infection (at the same levels as reported for A. brassicae). Germination also requires the presence of moisture in the form of free water or high relative humidity (at least 95%) (Degenhardt et al., 1982).
A. brassicae and A. brassicicola remain viable for a long period of time as spores on seed coat or as mycelium in seed as well as in infected plant debris. Twenty month-old seed samples infected with A. brassicae that were stored at 0 C for fourteen months showed high germinability. A. brassicae cultures exposed to outdoor weather for a six month period in which temperatures ranged from -23 to 30 C showed that the spores were still viable and pathogenic. These results, however, do not dictate the behavior of the organism in the soil (Rangel, 1945). Evidence that the fungus sometimes is carried as latent mycelium in the seed has been shown for seeds treated for surface spores that still produced symptoms of infection in seedlings (Rangel, 1945). Seeds infected with A. brassicicola are known to have active surface spores for up to 2 years when the seeds are stored at 10 C with 50% relative humidity. Internal mycelium can remain viable for up to 12 years (Maude and Humpherson-Jones, 1980a, b). Infected plant debris is also a major source of spores, which can survive up to 12 weeks. This is a potential problem for crops that are planted in a recently harvested field (Humpherson-Jones, 1989).
A. brassicae and A. brassicicola also survive in the form of microsclerotia and chlamydospores which appear after infected leaves have partially decayed (Tripathi and Kaushik, 1984). Microsclerotia and chlamydspores of both pathogens can be formed within conidial cells. Both microsclerotia and chlamydospores develop best at low temperatures (3 C) and are resistant to freezing and dessication (in vitro studies). Chlamydospores also can develop in conidial cells on natural soil at room temperature (Tsuneda and Skoropad, 1977).
Infected seeds, with spores on the seed coat or mycelium under the seed coat, are likely the main source of transport for these pathogens. Spores are disseminated by wind, water, tools and animals. The fungus can survive in susceptible weeds or perennial crops (Chupp and Sherf, 1960; Rangel, 1945; Maude and Humpherson-Jones, 1980a, b).
Infected crops left on the ground after harvest also serve as a source of infection for A. brassicae and A. brassicicola. In one study, infected leaves of oilseed rape and cabbage placed outdoors on soil, produced viable spores for as long as leaf tissues remained intact. For oilseed rape this was up to 8 weeks and for cabbage up to 12 weeks (Humpherson-Jones, 1989). This type of spread is likely to occur in seedling beds as well, and seedlings from infected seed beds can carry the inoculum to the field (Rangel, 1945).
In vitro studies have shown that there is a relationship between temperature and sporulation. If these relationships apply under field conditions, they may be of value in predicting sporulation and subsequent disease development of A. brassicae in a wide range of susceptible crops (Humpherson-Jones and Phelps, 1989).
Surface sterilization of seeds infected with A. raphani (3 min. in 4% sodium hypochlorite) reduced infection by 30% (Valkonen and Koponen, 1990).
Seed treatment with hot water is one method of controlling spores on the seed coat. However, this treatment sometimes depresses germination.
Rotation with noncruciferous crops and eradication of cruciferous weed hosts can help control these pathogens. Since spores can survive on leaf tissue for 8 to 12 weeks and stem tissue for up to 23 weeks, fields that are replanted soon after harvest often coincide with a large amount of inoculum which is likely to effect the crop's emergence and early growth stages (Humpherson-Jones, 1989).
Use of resistance:
Cultivars of Brassica species differ in resistance to A. brassicae but differences are not large (Bansal et al., 1990).
Preliminary studies with the actinomycete fungus, Streptomyces arabicus, indicated an antifungal effect on A. brassicae and A. brassicicola in both laboratory and field studies (Sharma et al., 1984; Sharma et al., 1985). In Finland, surface treatment with powdered S. griseoviridis (at 15 mg/g seed) has been shown to provide control against A. brassicicola, but does not control A. raphani, which infects the inner part of seed (Valkonen and Koponen, 1990). Further work is needed before this nonchemical approach may be practical.
Many fungicides have been tested for effectiveness in controlling A. brassicae and conclusions are often conflicting. Ansari et al. (1990) evaluated eighteen fungicides as to their control of A. brassicae in artificial cultures, infected seeds, and as a foliar spray on infected plants of B. campestris var. yellow sarson (a highly susceptible rape cultivar). Throughout the study Dithane M-45 (Mancozeb) and Dithane Z-78 (Zineb) consistently provided the best control data. Seven fungicides completely inhibited the growth of the pathogen in culture: Benlate at 0.1 lb a.i./100 gal, Dithane M-45, Dithane Z-78, Ziram, Difolatan-80 and Thiram (all at 0.2 lb a.i./100 gal), and Blitox-50 at 0.3 lb a.i./100 gal. As a seed dressing, Benlate at 0.1 lb a.i./100 lb seed provided the best control with a mean loss of 4.5 pre-emergence seedlings and 6.5 post-emergence seedlings per pot (25 seeds planted in each pot, 8 pots). Dithane M-45 and Dithane Z-78, both applied at 0.2 lb a.i./100 lbs seed, had a mean pre-emergence seedling loss of 10.5 and 11.25, respectively and post-emergence seedling loss of 11.5 and 13.75, respectively. As a foliar spray, Dithane M-45 (0.2 lb a.i./100 gal) provided significantly better control over other fungicides, including Benlate. Dithane M-45 gave better results than Dithane Z-78 (0.2 lb a.i./100 gal), although the difference was not significant. Plants treated with these two fungicides also provided the highest seed yields.
Iprodione and fenpropimorph have both shown high inhibitory properties to the growth of Alternaria sp. in culture and as seed treatments at 0.25 lb a.i./100 lb seed (Maude et al., 1984). In seed samples with up to 61.5% infection (35.5% internally diseased), iprodione usually eliminated the fungus from the sample, but higher levels of infection required a larger dose of iprodione. The germination of healthy seeds was unaffected by treatment, and diseased seed germination improved (Maude and Humpherson-Jones, 1980a, b).
Surface treatment with thiram at 0.55 lb/100 lb seed controlled A. brassicicola, but did not control internal infections of A. raphani (Valkonen and Koponen, 1990).
Ansari, N.A., M. Wajid Kahn, and A. Muheet. 1990. Evaluation of some fungicides for seed treatment and foliar application in management of damping-off of seedlings and blight of rapeseed caused by Alternaria brassicae. Mycopathologia 110:163-167.
Bansal, V.K., G. Seguin-Swartz, G.F.W. Rakow, and G.A. Petrie. 1990. Reaction of Brassica species to infection by Alternaria brassicae. Can. J. Plant Sci. 70:1159-1162.
Bassey, E.O., and R.L. Gabrielson. 1983. The effects of humidity, seed infection level, temperature and nutrient stress on cabbage seedling disease caused by Alternaria brassicicola. Seed Sci. & Technol. 11:403-410.
Chupp, C., and A.F. Sherf. 1960. Vegetable diseases and their control. Pp. 267-269. The Ronald Press Company. New York. 693 pp.
Degenhardt, K.J., G.A. Petrie, and R.A.A. Morrall. 1982. Effects of temperature on spore germination and infection of rapeseed by Alternaria brassicae, A. brassicicola, and A. raphani. Can. J. Plant Pathol. 4:115-118.
Humpherson-Jones, F.M. 1989. Survival of Alternaria brassicae and Alternaria brassicicola on crop debris of oilseed rape and cabbage. Ann. appl. Biol. 115:45-50.
Humpherson-Jones, F.M., and K. Phelps. 1989. Climatic factors influencing spore produciton in Alternaria brassicae and Alternaria brassicicola. Ann. appl. Biol. 114:449-458.
Maude, R.B., and F.M. Humpherson-Jones. 1980a. Studies on the seed-borne phases of dark leaf spot (Alternaria brassicicola) and grey leaf spot (Alternaria brassicae) of brassicas. Ann. appl. Biol. 95:331-319.
Maude, R.B., and F.M. Humpherson-Jones. 1980b. The effect of iprodione on the seed-borne phase of Alternaria brassicicola. Ann. appl. Biol. 95:321-327.
Maude, R.B., F.M. Humpherson-Jones, and C.G. Shuring. 1984. Treatments to control Phoma and Alternaria infections of brassica seeds. Plant Pathology 33:525-535.
Rangel, J.F. 1945. Two Alternaria diseases of cruciferous plants. Phytopathology 35:1002-1007.
Sharma, A.K., J.S. Gupta, and R.K. Maheshwari. 1984. The relationship of Streptomyces arabicus to Alternaria brassicae (Berk.) Sacc. and Alternaria brassicicola (Schew.) Wiltshire on the leaf surface of yellow sarson and taramira. Geobios New Reports 3:83-84.
Sharma, A.K., J.S. Gupta, and S.P. Singh. 1985. Effect of temperature on the antifungal activity of Streptomyces arabicus against Alternaria brassicae (Berk) Sacc. and A. brassicicola (Schew.) Wiltshire. Geobios 12:168-169.
Tripathi, N.N., and C.D. Kaushik. 1984. Studies on the survival of Alternaria brassicae the causal organism of leaf spot of rapeseed and mustard. Madras Agric. J. 71:237-241.
Tsuneda, A. and W.P. Skoropad. 1977. Formation of microsclerotia and chlamydospores from conidia of Alternaria brassicae. Can. J. Bot. 55:1276-1281.
Valkonen, J.P.T., and H. Koponen. 1990. The seed-borne fungi of Chinese cabbage (Brassica pekinensis), their pathogenicity and control. Plant Pathology 39:510-516.