Plasmopara halstedii. [Descriptions of Fungi and Bacteria].

Author(s):  
G. Hall

Abstract A description is provided for Plasmopara halstedii. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Over 80 hosts from a wide range of genera in the Compositae have been reported, including wild and cultivated species of Helianthus. For lists see Leppik (1966) and Novotel'nova (1977). DISEASE: Downy mildew of sunflower (Helianthus annuus var. macrocarpus); the fungus is an obligately biotrophic plant pathogen. Leaves of infected plants develop chlorotic mottling which spreads from the veins near the petiole across the lamina, and increases in area and intensity as leaves age. Plants become stunted, having thin stems, very much smaller capitula without seeds, and smaller and darker roots. The disease is primarily systemic and mycelium can be found throughout the plant from roots to capitulum and achenes, in all except meristematic tissues. Under humid conditions, a white felt of sporangiophores develops on the undersurface of chlorotic areas. Localized secondary infection of the leaves and heads occasionally develops, resulting in spots, delimited by veins. Such secondary infection may also become systemic. Some infected plants show no disease symptoms, but produce lower yields of poorer quality seeds, which lose vitality and have lower germination rates (latent infection). Cotyledons are also infected causing damping-off in seed beds. A basal gall may also be produced. GEOGRAPHICAL DISTRIBUTION: Plasmopara halstedii is a fungus characteristic of the Americas, its putative origin, It has spread throughout Europe to parts of Africa and Asia, and has recently been reported from New Zealand. See CMI Distribution Maps of Plant Diseases 286. TRANSMISSION: Soil-borne oospores and mycelium (in systemically infected roots) overwinter, infecting subsequent crops. Sporangia form on the surface of infected seedling roots, releasing zoospores which encyst and germinate c root hairs of other seedlings, producing a systemic infection. Sporangia are dispersed by rain-splash from leaves, producing a secondary infection in plants up to the six-leaf stage, but infect only the apical growing points of olde plants. Transmission by oospores in seeds has been responsible for the spread of this fungus around the world, especially since these spores can germinate to produce only a latent infection in the host plant (53, 4545).

Author(s):  
G. Hall

Abstract A description is provided for Plasmopara viticola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Ampelopsis brevipedunculata, A. hederacea, A. heterophylla, A. veitchii, Ampelocissus acetosa, A. latifolia, A. salmonea, Cissus caesia, C. gracilis, C. hypoglauca, C. polyantha, Cordifolia sempervirens, Cinerea sp., Parthenocissus quinquefolia, P. tricuspidata, Solonis robusta, Vitis aestivalis, V. amurensis, V. arizonica, V. berlandieri, V. californica, V. cinerea, V. coignetiae, V. cordifolia, V. girdiana, V. labrusca, V. lanata, V. monticola, V. pagnuccii, V. riparia, V. romaneti, V. rupestris, V. silvestris, V. treleasei, V. vinifera. DISEASE: Grape vine downy mildew; the fungus is an obligately biotrophic plant pathogen. All tissues bearing stomata are infected, becoming discolored, malformed and necrotic. Lesions on affected organs develop a white felt of sporangiophores. Leaves are most susceptible to attack during active growth in early summer, and when very mature in the autumn. Sporangiophores may appear directly on healthy green leaf tissues with no overlying lesion, or as a dense felt under yellow oily lesions on the upper surface (if humidity is high, 5-15 days after infection), or may be absent, leaves presenting only a mosaic of small, angular yellow or dark-red blemishes, limited by the secondary veins (mainly on old leaves in the autumn). During early growth, whole branches are attacked, but later only the extremities of branches are invaded. Infected shoots turn brown, curl up or become hooked at their tips. Nodes are more susceptible to attack than internodes. Tendrils, petioles, inflorescences and bunches also develop similar brown spots and lesions. Bunches are susceptible until the grapes are 5-6 mm diam., after which infection is rare (grey rot followed later by brown rot). Subsequent browning and desiccation of the bunch is caused by penetration of the bunch stalk by mycelium from earlier infections elsewhere. GEOGRAPHICAL DISTRIBUTION: See CMI Distribution Maps of Plant Diseases 221. TRANSMISSION: Oospores present in infected leaf tissues from the previous season's crop germinate in the spring, when air temperatures exceed 12°C and at least 10 mm rain falls in 24 hours, releasing zoospores into water or onto very moist soil from sporangia (64, 2458). Zoospores are projected onto vine leaves near the soil by rain splash, germinate to give hyphae and penetrate tissues via their stomata. Sporangia are liberated in moist air only, are disseminated by air currents, and remain viable for five days in dry air, producing secondary infection sites. Production of sporangia occurs at a relative humidity of 95-100%, and an air temperature of 13-27°C (optimum 18-22°C). Mycelium may overwinter between the bud scales and in diseased leaves, but it has not been established whether this contributes substantially to re-infection of healthy leaf tissues the following spring. There is no evidence for systemic transmission.


Author(s):  
J. C. David

Abstract A description is provided for Passalora sojina. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Frog-eye leafspot. HOSTS: Glycine hispida, G. javanica, G. max, G. soja, G. ussuriensis (FALEEVA, 1976), Mucuna sp. (CROUS & BRAUN, 2003) (Fabaceae). GEOGRAPHICAL DISTRIBUTION: [CAB International Distribution Maps of Plant Diseases No. 871, Edn. 1 (2002)]. AFRICA: Cameroon, Côte d'Ivoire, Egypt, Gabon, Kenya, Malawi, Nigeria, Zambia, Zimbabwe. NORTH AMERICA: Canada (Ontario), Mexico, USA (Alabama, Arkansas, Delaware, Florida, Georgia, Hawaii, Illinois, Indiana, Iowa, Kansas, Louisiana, Maryland, Michigan, Mississippi, Missouri, New Jersey, New York, North Carolina, Oklahoma, South Carolina, Texas, Virginia, West Virginia, Wisconsin). CENTRAL AMERICA: Cuba, Guatemala. SOUTH AMERICA: Argentina, Bolivia, Brazil (Goias, Maranhao, Mato Grosso, Minas Gerais, Parana, Pernambuco, Piaui, Rio Grande do Sul, Santa Catarina, Sao Paolo), Venezuela. ASIA: China (Fujian, Gansu, Guangxi, Hebei, Heilongjiang, Henan, Jiangsu, Jiangxi, Jilin, Liaoning, Nei Menggu, Sichuan, Yunnan, Zhejiang), East Timor, India (Karnataka, Meghalaya, Sikkim, Uttar Pradesh), Japan, Nepal, Russia (Far East), South Korea, Taiwan. EUROPE: Russia. TRANSMISSION: Seedborne and by aerial dispersal of conidia through wind and rain splash. The fungus also survives in dead plant material and can re-infect living plants (SWEETS, 2001).


Author(s):  
M. A. J. Williams

Abstract A description is provided for Sclerotinia narcissicola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Narcissus spp. DISEASE: Smoulder, grey mould. Infection may reduce bulb yield and flower size (55, 3617). Symptoms may include: rot of the bulbs and leaves at ground level, brown lesions on the leaves and flower buds, distortion and failure of emergence. GEOGRAPHICAL DISTRIBUTION: Asia: Iraq, USSR; Australasia: Australia (Tasmania, Victoria), New Zealand; Europe: Channel Islands (Guernsey, Jersey), Denmark, Eire, England, Germany, Northern Ireland, The Netherlands, Norway, Scotland, Sweden, USSR, Wales, West Germany; North America: Canada (British Columbia, NS, Ontario, PEI); USA (North Carolina, New York, Oregon, Virginia, Washington State) (see CMI Distribution Maps of Plant Diseases, No. 315). TRANSMISSION: The disease may come from planting of infected bulbs or from infected soil; sclerotia in the soil may be viable for up to nine months (61, 7053). In vitro conidial suspensions did not cause infection except of wounded or damaged tissue; mycelial inoculation consistently caused lesions on detached leaves and bulb scales (61, 5797).


Author(s):  
V. P. Hayova

Abstract A description is provided for Valsa sordida. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Valsa sordida is usually associated with Valsa canker of poplar twigs. Wounded trees, and trees injured by insects or attacked by other pathogens are more susceptible to infection. Development of Valsa canker is affected by environmental stress (Guyon, 1996; Tao et al., 1984). Poplar canker caused by V. sordida has been studied in different countries (CMI Distribution Maps of Plant Diseases, 1977; Worrall, 1983; Wang et al., 1981) The fungus can be often found in declining poplar stands together with another pathogen of poplar trees, Leucostoma niveum. Valsa sordida may also cause necrosis of willow twigs. HOSTS: Populus spp., Salix spp. and, more rarely, other woody angiosperms. GEOGRAPHICAL DISTRIBUTION: Africa: Morocco. Asia: Armenia, Azerbaijan, China, Republic of Georgia, India, Iran, Iraq, Israel, Japan. Kazakhstan, Korea, Russia (Tatarstan), Turkey, Turkmenia, Uzbekistan. Australasia: Australia (Victoria), New Zealand. Europe: Austria, Belgium, Bulgaria, Czech Republic, Denmark, Estonia, France, Germany, Greece, Ireland, Italy, Netherlands, Norway, Poland, Portugal, Rumania, Russia, Slovakia, Sweden, Switzerland, UK, Ukraine, former Yugoslavia. North America: Canada (Alberta, British Columbia, Nova Scotia, Ontario, Québec, Saskatchewan). USA (California, Colorado, Michigan, Minnesota). South America: Chile. TRANSMISSION: Both conidia and ascospores are air-borne, especially under humid conditions. Yellow or orange exudation of conidia from conidiomata can be often seen after rain.


Author(s):  
J. M. Pérez

Abstract A description is provided for Sporisorium sorghi. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. DISEASE: Covered smut or covered kernel smut of sorghum. Development of functional ovaries and anthers is prevented in infected parts of the plants. HOSTS: Panicum miliaceum, Sorghum bicolor, S. dochna, S. halepense, S. plumosum, S. sudanense and S. vulgare (Poaceae). This species has also been recorded from Ischaemum ciliare (VISWANATHAN et al., 2000). GEOGRAPHICAL DISTRIBUTION: Worldwide, see CMI Distribution Maps of Plant Diseases No. 220, edn 4 (1987). In addition it has been recorded from AFRICA: Mauritania (FRISON & SADIO, 1987). CENTRAL AMERICA: Nevis. TRANSMISSION: In addition to dissemination on infected seed, there is evidence that this species can also be spread by air-borne chlamydospores (SHENOI & RAMALINGAM, 1976).


Author(s):  
C. Booth

Abstract A description is provided for Fusarium culmorum. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On Gramineae and a wide range of other plant species including the following families: Aizoaceae, Betulaceae, Brassicaceae, Campanulaceae, Caryophyllaceae, Chenopodiaceae, Compositae, Coniferae, Convolvulaceae, Cucurbitaceae, Leguminosae, Liliaceae, Linaceae, Malvaceae, Musaceae, Palmae, Rosaceae, Saxifragaceae, Solanaceae, Violaceae, Vitaceae. Also on fungi (Agaricus and Ustilago spp.) [Wollenweber & Reinking (1935), Gordon (34: 258; 38: 581; 40: 89) and Herb. IMI]. DISEASES: Causing cortical rots associated with a pre-emergence blight of seedlings, and a seedling blight, foot and root rot, and head blight of wheat, rye, oats and barley; also cob and stem rot of maize; brown patch of turf; foot rot of asparagus, carnation, leek and pea; and storage rots of apple, potato, sugar-beet and Galtonia bulbs. GEOGRAPHICAL DISTRIBUTION: Africa, North America, Central America & West Indies, South America, Asia, Australasia, and Europe. TRANSMISSION: Mainly soil-borne but also in stable manure or compost containing infected straw (13: 23; 14: 735; 19: 649). Fusarium culmorum is a soil inhabitant possessing highly competitive saprophytic ability and unusual tolerance of antibiotic effects [see Garrett (1956, 1963); Rao (1959); 34: 147; 38: 577)]. It may occur in a viable condition in soil to a depth of 50 cm. (19: 11; 13: 23), and remain viable on wheat straw buried in unsterilized soil for 2 years (38: 509). The pathogen over-winters in both mycelial and conidial stages and is highly resistant to cold (17: 305, 306). Secondary infection by air-borne spores produced on lower nodes occurs in wet weather (3: 201; 7: 710; 9: 585), but these are not carried far and have not been recorded in traps (15: 384; 38: 319).


Author(s):  
G. Hall

Abstract A description is provided for Aphanomyces cladogamus. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Capsicum sp., Lactuca saliva, Linum sp., Lycopersicon esculenteum, Raphanus sativus, Solanum melongena, Spinacea oleracea, Viola tricolor. DISEASE: Root rot of pepper, spinach, pansy, tomato and several other crop and garden plants. The fungus, a facultatively necrotrophic plant pathogen, attacks seeds (pre-emergence disease) and/or seedlings (post-emergence damping off). Affected plants develop a generalized wilt which becomes progressively more severe. In pepper, seeds are attacked and black lesions develop on hypocotyls of the surviving seedlings, often extending to the bases of the cotyledons (32, 360). In spinach, roots become covered in yellow to orange spots their tissues becoming soft and water-soaked. In pansies, the vascular cylinder develops a deep orange-reddish discoloration in which, in the early stages of infection, numerous oospores can be seen. Stem bases become extensively rotted and eventually the aerial organs collapse and shrivel (13, 379; 34, 370). In tomato plants, rootlet tips become discoloured and die back (6, 517). GEOGRAPHICAL DISTRIBUTION: Europe: Sweden. North America: Canada (Ontario), USA (MD, NC, NJ, VA, WA, WI). See CMI Distribution Maps of Plants Diseases 601. TRANSMISSION: Not reported. Presumably by zoospores and oogonia remaining in infected tissues. As the fungus appears to infect a wide range of plants, it may persist in the roots of weeds.


Author(s):  
G. Hall

Abstract A description is provided for Peronospora rubi. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Rubus arcticus, R. caesius, R. canadensis, R. canescens, R. chamaemorus, R. cissiburiensis, R. cissoides, R. corylifolius egg. (R. caesius × tereticaulis, R. nemorosus), R. flagellaris, R. fruticosus egg. (R. bregutiensis, R. buschi, R. glandulosus, R. hirtus, R. menkei, R. seebergensis, R. tereticaulis, R. vulgaris), R. idaeus, R. laciniatus, R. leucodermis, R. × loganobaccus (orursinus × ideaus), R. occidentalis, R. parviflorus, R. plicatus, R. procerus, R. spectabilis, R. strigosus, R. sulcatus, R. tuberculatus, R. villosus, R. vitifolius, and certain hybrids, e.g. 'Tayberry' (blackberry cv. Aurora × tetraploid red raspberry), 'Tummelberry' (a 'Tayberry' interspecific cross) and 'Youngberry'. DISEASE: Downy mildew of cane fruits (Rubus spp.), especially blackberry (R. fruticosus agg.), boysenberry (a blackberry × red raspberry cross: the name R. × loganobaccus covers this plant) and raspberry (R. idaeus). The fungus, an obligately biotrophic plant pathogen, occurs on leaves in summer to autumn, producing small, conspicuous, irregularly shaped patches on upper leaf surfaces, starting near the petiole, then following leaf veins. Patches are initially yellow, becoming carmine-red, vinaceous or purple and are bordered by venation. The undersurface of the leaf shows only a pale area with a brownish edge, and brownish discoloration near and alongside veins. Sporophores are sometimes difficult to detect in the dense mat of leaf hairs, but are heaviest on lowest leaves, close to ground level, forming a buff-grey felt. In wild-growing European species of Rubus the fungus occurs exclusively on the leaves. In North America it attacks leaves of cultivated raspberry bushes, and in New Zealand the fruits, sepals and pedicels of boysenberry, causing the fruit to become dry and shrivelled (dryberry disease). Downy mildew has recently become a problem on certain berry cultivars in Eastern England (McKeown, 1988). GEOGRAPHICAL DISTRIBUTION: Africa: South Africa. Asia: USSR (Azerbaijan). Australasia & Oceania: New Zealand. Europe: Czechoslovakia, Denmark, Finland, France, Germany (GFR, GDR), Norway, Poland, Rumania, Sweden, Switzerland, United Kingdom, USSR (Latvia). North America: Canada (British Columbia), USA (IL, MD, OR, WA, WI). See CMI Distribution Maps of Plant Diseases 598. TRANSMISSION: Determined for boysenberry in New Zealand only (61, 4245), where it is a systemic disease confined to the outer cortex parenchyma, keeping pace with cell division at apical meristems. Systemic cane infection is often indicated by red streaking of stems and petioles linking successively diseased leaves on a shoot. Unfolding leaves are invaded during warm wet weather causing typical leaf symtoms. Stores produced on diseased shoots initiate secondary infections of flowers and developing berries. These berries then become an important source of inoculum for new cycles of the disease. They go largely unnoticed, since spores are partially hidden on the split berry surfaces or covered by the sepals. After harvest, infection of developing primocanes continues by internal mycelial growth and spore infection. Oospores form on root surfaces in dead cortex cells and leaves. Soilborne oospores may infect healthy plants established in former sites of infected root crowns.


Author(s):  
G. Hall

Abstract A description is provided for Aphanomyces cochlioides. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Amaranthus blitoides, A. retroflexus, Beta lomatogona, B. patellaris, B. patula, B. trigyna, B. vulgaris, B. vulgaris var. cicla, Celosia argentea, Chenopodium album, Dianthus chinensis, Echinocloa crus-gallii, Escholtzia californica, Gomphrena globosa, Kochia scoparia, K. scoparia var. culta, Lychnis alba, Mollugo verticillata, Papaver rhoeas, Portulaca oleracea, Salsola kali, Saponaria ocymoides, Spinacia oleracea, Tetragonia tetragonioides. DISEASE: Blackroot of sugar beet; the fungus is a facultatively necrotrophic plant pathogen. There is an early acute phase of short duration (causing pre-emergence and post-emergence damping off) and a later chronic phase which may persist throughout the life of the plant. Infection during seed germination is indicated by poor stands with killed seeds remaining in the soil to infect young seedlings emerging elsewhere. Seedling hypocotyls are infected at ground level, a water-soaked area extending up and down the hypocotyl or the upper part of the young taproot from the point of entry. The invaded root or hypocotyl rapidly becomes brownish and then assumes the characteristic jet black discoloration from which the disease derives its name. Soon after, the cortex of the hypocotyl dries, and the stem and hypocotyl shrink, leaving a thin strand of tissue. Oospores are easily seen in the collapsed root and hypocotyl tissue on microscopic examination. The chronic phase first appears on plants in late June to August. A greenish-yellow discoloration of the swollen hypocotyl develops, affected root tissues becoming dark brown, soft, water-soaked, splitting apart and eventually shrivelling. Plants are stunted and lower leaves turn yellow. GEOGRAPHICAL DISTRIBUTION: Asia: Japan. Australasia & Oceania: Australia (Qld). Europe: Austria, Denmark, England, France, Germany (GDR & GFR), Hungary, Ireland, Poland, Sweden, USSR (Russia). North America: Canada (Alberta, NS, Ontario, Quebec), USA (California, Connecticut, Indiana, Michigan, Maine, MT, North Dakota, Ohio, South Dakota, Texas, Washington State, Wisconsin). South America: Chile. See CMI Distribution Maps of Plant Diseases 596. TRANSMISSION: Presumably in soil by oospores originating from sloughed-off root tissues and germinating to produce zoospores. The conditions favouring oospore germination are however largely unknown. Survival may occur on alternative hosts present in the crop, so the disease may be difficult to eliminate. The disease is particularly severe in warm, wet conditions, less so in cool, wet weather.


1974 ◽  
Vol 52 (1) ◽  
pp. 231-238 ◽  
Author(s):  
Yigal Cohen ◽  
W. E. Sackston

Sunflowers bud-inoculated with Plasmopara halstedii became systemically infected with downy mildew and produced infected seeds at 15 to 30 °C. Oospores were observed in seeds of inoculated and also naturally infected plants from the field. Infected seeds gave rise to symptomless plants. Infected seeds proved effective as inoculum, inducing infection in 14 to 89% of the plants inoculated at 20 °C. Most of the infections (80%) were symptomless (latent).Systemic infection occurred, but latent infection was more frequent, in plants grown in soil containing debris of mildewed plants. Latent infection also occurred in uninoculated plants through belowground contact with systemically infected plants. Seed produced by plants with latent infection may carry the pathogen, and may give rise to more plants with latent infection, accounting for widespread dissemination of the disease before plants with typical symptoms are observed.


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