Sclerotinia trifoliorum. [Descriptions of Fungi and Bacteria].

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).

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):  
M. A. J. Williams

Abstract A description is provided for Sclerotinia borealis. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Lolium perenne and various cereals, forage grasses and lawn grasses (including Triticum cultivars, Phleum pratense, Agrostis tenuis, Alopecurus pratensis, Anthoxanthum odoratum, Bromus inermis, Dactylis glomerata, Festuca spp., Poa pratensis, Secale cereale). DISEASE: Snow scald, snow mould. GEOGRAPHICAL DISTRIBUTION: Asia: Japan, USSR; Europe: Finland, Norway, Sweden, USSR; North America: Canada (Alberta, British Columbia, Manitoba, Saskatchewan, Yukon); United States (AK, MN, WA) (see CMI Distribution Maps of Plant Diseases, No. 446). TRANSMISSION: Penetration of the fungus has been shown to occur (in vitro) through stomata and intercellularly. In the field disease entry can be facilitated by injury which is increased by slight freezing of the soil, a thick snow cover and slow melting of the snow in the spring. Sclerotia develop within the culms, digesting and to some extent incorporating the host tissue. Sclerotia may also be present on the leaves. Germination of sclerotia occurs to produce apothecia, with the subsequent production of ascospores which may then become the infective agents. The development of apothecia and the dissemination of ascospores are favoured by long, rainy autumns.


BioControl ◽  
2021 ◽  
Author(s):  
Mudassir Iqbal ◽  
Maha Jamshaid ◽  
Muhammad Awais Zahid ◽  
Erik Andreasson ◽  
Ramesh R. Vetukuri ◽  
...  

AbstractUtilization of biocontrol agents is a sustainable approach to reduce plant diseases caused by fungal pathogens. In the present study, we tested the effect of the candidate biocontrol fungus Aureobasidium pullulans (De Bary) G. Armaud on strawberry under in vitro and in vivo conditions to control crown rot, root rot and grey mould caused by Phytophthora cactorum (Lebert and Cohn) and Botrytis cinerea Pers, respectively. A dual plate confrontation assay showed that mycelial growth of P. cactorum and B. cinerea was reduced by 33–48% when challenged by A. pullulans as compared with control treatments. Likewise, detached leaf and fruit assays showed that A. pullulans significantly reduced necrotic lesion size on leaves and disease severity on fruits caused by P. cactorum and B. cinerea. In addition, greenhouse experiments with whole plants revealed enhanced biocontrol efficacy against root rot and grey mould when treated with A. pullulans either in combination with the pathogen or pre-treated with A. pullulans followed by inoculation of the pathogens. Our results demonstrate that A. pullulans is an effective biocontrol agent to control strawberry diseases caused by fungal pathogens and can be an effective alternative to chemical-based fungicides.


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):  
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.


2021 ◽  
Author(s):  
Mudassir Iqbal ◽  
Maha Jamshaid ◽  
Muhammad Awais Zahid ◽  
Erik Andreasson ◽  
Ramesh R. Vetukuri ◽  
...  

Abstract Utilization of biocontrol agents is a sustainable approach to reduce plant diseases caused by fungal pathogens. In the present study, we tested the effect of the candidate biocontrol fungus Aureobasidium pullulans (De Bary) G. Armaud on strawberry under in vitro and in vivo conditions to control, crown rot, root rot and grey mould caused by Phytophthora cactorum (Lebert and Cohn) and Botrytis cinerea Pers respectively. A dual plate confrontation assay showed that mycelial growth of P. cactorum and B. cinerea was reduced by 33- 48% when challenged by A. pullulans as compared with control treatments. Likewise, detached leaf and fruit assays showed that A. pullulans significantly reduced necrotic lesion size on leaves and disease severity on fruits caused by P. cactorum and B. cinerea . In addition, greenhouse experiments with whole plants revealed enhanced biocontrol efficacy against root rot and grey mould when treated with A. pullulans either in combination with the pathogen or pre-treated with A. pullulans followed by inoculation of the pathogens. Our results demonstrate that A. pullulans is an effective biocontrol agent to control strawberry diseases caused by fungal pathogens and can be an effective alternative to chemical-based fungicides.


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