Aphanomyces raphani. [Descriptions of Fungi and Bacteria].

Author(s):  
G. Hall

Abstract A description is provided for Aphanomyces raphani. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Species in the Cruciferae only. Brassica alboglabra, B. carnet, B. campestris var. pekinensis, B. chinensis, B. juncea, B. napobrassica, B. napus, B. nigra, B. oleracea (vars acephala, botrytis, capitata, gemmifera, gongylodes, italica, viridis), B. perviridis, B. rapa, B. robertiana, Crambe abyssinica, Eruca saliva, Lunaria annua, Raphanus raphanistrum, R. sativus, Sinapis alba. DISEASE: Black-root disease of radish; the fungus is a facultatively necrotrophic plant pathogen. Small black, water-soaked lesions on the lower hypocotyl and epidermis accompanied by slight longitudinal cracking of the subepidermal tissues become visible 20 days after sowing. In seedlings, the roots, hypocotyls, petioles and cotyledons become blackened and collapse. On older plants horizontal spread of the fungus produces characteristic constrictions and irregular bands around the circumference of the root (girdle disease). Subsequent penetration of the inner cortex results in blackening of the internal tissues in a portion or all of the root, accompanied by deformity of the roots and stunting of the tops due to retardation of growth. Lesions become invaded rapidly by secondary colonisers such as soft-rot bacteria. GEOGRAPHICAL DISTRIBUTION: Africa: South Africa. Asia: Japan. Australasia & Oceania: Australia (NSW Qld), New Zealand. Europe: Germany, Rumania. North America: Canada (British Columbia, NS, Ont, Que), USA (California, IL IA, IN, ME to Florida, OR). South America: Venezuela. See CMI Distribution Maps of Plant Diseases 421. TRANSMISSION: In wet soil, by zoospores which accumulate at root tips in response to hypocotyl exudates or indole-3-aldehyde (59, 3937). The large number of crucifers (particularly cole crops) infected by A. raphani allows it to persist even in the absence of a radish crop. Oospores are generally believed to survive in soil, although there is no evidence to support this. The oospore germinates via a hypha which produces an apical sporangium.

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):  
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 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.


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):  
G. Hall

Abstract A description is provided for Peronophythora litchii. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Litchi chinensis. Peronophythora litchii also infected artificially inoculated fruits of tomato, pawpaw and loofah (Luffa cylindrica[Luffa aegyptiaca])(64, 1198). DISEASE: Fruit rot or downy blossom blight of lychee (litchi); the fungus is a facultative necrotrophic plant pathogen. Diseased flowers turn brown and become covered with whitish masses of sporangia and sporangiophores. Young and ripe fruits, pedicels and leaves are also attacked, their tissues turning brown and dying, especially in periods of heavy rain (64, 688). The infection period was shown in laboratory studies to be fast and temperature dependent, varying from 1 day at 25°C to 3 days at 18°C (64, 1198). Continuous rain in the growing season in May appears important for development of an epiphytotic. GEOGRAPHICAL DISTRIBUTION: Asia: China (Guangdong), New Guinea, Taiwan. See CMI Distribution Maps of Plant Diseases 597. TRANSMISSION: Sporangia not liberated by moving air, but readily dispersed in splash droplets, suggesting a rain-splash mechanism.


Author(s):  
M. A. J. Williams

Abstract A description is provided for Sclerotinia trifoliorum. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Trifolium spp., also Medicago sativa and other herbaceous leguminous forage crops including Anthyllis vulneraria, Lathyrus spp., other Medicago spp., Melilotus spp. and Vicia spp. including V. faba (on this host causing 'Bean rot'; the causal agent of which has often been referred to as S. trifoliorum var. fabae Keay) and V. saliva. Although approximately 100 hosts have been recorded for this pathogen there is often a lack of conclusive evidence that S. trifoliorum and not another Sclerotinia species is to blame. DISEASE: Rot, called variously: Stem rot, Crown rot, Brown patch of lawns, Clover sickness, Clover canker. Symptoms include leaf rot, petiole rot and stem rot. Initial leaf spotting may be followed by these more severe rot symptons. The foliage usually turns grey-green as though scalded, then may wither and the rot may spread. In lucerne the leaves may be totally destroyed by the pathogen, but it takes a long time to reach the root system through the comparatively thick stem. TRANSMISSION: The development of apothecia occurs in the autumn. Ascospores infect the leaves, and rotting of the clover plants sets in the following early spring. The fungus is able to complete its entire life-cycle as a saprophyte. Spread from plant to plant takes place chiefly along affected petioles, but the pathogen may grow about 2 cm over the soil from a nutritional base. The fungus can persist in the crown of the plant throughout the summer until harvest. Sclerotia may germinate to produce apothecia and ascospores which may infect emergent shoots; sclerotial germination is favoured by light, well-aerated soils and a temperature between 10° and 20°C. Mycelium and ascospores remain viable (in a dry state) for seven months, sclerotia buried in the soil survive for more than seven years. In vitro conidia will infect clover plants. GEOGRAPHICAL DISTRIBUTION: Africa: Egypt; Asia: China, India, Israel, Japan, Korea; Australasia & Oceania: Australia (NSW, Viet., Tas., W.A.), New Zealand; Europe: Austria, Belgium, Bulgaria, Czechoslovakia, Denmark, Eire, Finland, France, Germany, Greece, Hungary, Italy, The Netherlands, Norway, Poland, Romania, Sweden, Switzerland, UK, USSR; North America: Canada (Alberta, British Columbia, Manitoba, Que, PEI), USA (widespread), Mexico; Central & South America: Chile (see CMI Distribution Maps of Plant Diseases No. 274).


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