This presentation provides you the necessary basic details on potato wart caused by Synchytrium endobioticum
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POTATO WART ( Synchytrium endobioticum ) Course teacher: Submitted by: Dr. S. Parthasarathy , Ph.D . Mr. Rohith A K Asst. Professor ( Plant Pathology) 2015021109 College of Agricultural Technology Theni
Occurrence and Distribution Synchytrium endobioticum originated in the Andean zone of South America. It was introduced from there into the UK and from there to continental Europe in the 1880s, and into North America ( New found land ) in the 1900s. It spread widely throughout the UK and the European continent in the early decades. The introduction of statutory measures limited its distribution, and it has spread to a limited extent only in other parts of the world . Synchytrium endobioticum occurs locally in almost all countries in the EPPO region . In India it is restricted distribution.
Losses In the 1950s and 1960s numerous EPPO publications were devoted to the disease. Once the pathogen has been introduced to a field of potato cultivation the whole crop may be devastated and unmarketable. Moreover , introduction into the soil not only renders the crop unusable but the soil itself cannot be used for further crop production due to the longevity of the fungus. Crops other than potato grown in this soil cannot be used for export . Indirect losses arising from restrictions on the export of plants from infested areas present a problem to European countries.
Hosts / Species affected The only cultivated host is potato, but wild species of Solanum are also infected in Mexico. Tomato and a number of other solanaceous plants, including Schizanthus sp., Capsicastrum nanum , Physalis franchetii , Datura sp. and Solanum dulcamara are hosts by artificial inoculation. Post-harvest, vegetative growing stage are mostly affecting period
Symptoms Aerial symptoms Aerial symptoms are not usually apparent. Reduction in vigor. Warts can be found in severe attacks on the upper stem, leaf and flower. Leaf stalks may develop hypertrophic 'wings'. Above-ground galls are green to brown, turning black at maturity, and later decaying.
Subterranean symptoms Galls vary in shape but are mostly spherical, with corrugated surfaces, and range from pea-size to fist-size <1 cm to >8 cm diam.). Ground galls are white to brown, turning black as they decay. These galls appear at stem bases, stolon tips and tuber eyes. At harvest , galls may desiccate or decay. Tubers may be disfigured or completely replaced by galls. Tuber galls may develop after harvest, in storage.
S tages of Potato wart on tuber
Wart attack on tubers and stolons
Symptoms on stem base
Leaf symptoms
Pathogen - Synchytrium endobioticum Synchytrium endobioticum is an obligate , holocarpic E ndobiotic parasite . It is long-cycled chytrid which does not produce hyphae but a thallus comprised of sporangia . Two forms of sporangia exist, so-called summer and winter sporangia (resting spores), which contain 200-300 motile zoospores . Synchytrium endobioticum develops no mycelium. Sporangia are clustered into thin-walled soruses . The motile life stage, zoospore is about 0.5 µm in diameter and has one posterior flagellum.
Disease Cycle In the spring, resting sporangia in decaying warts and soil germinate to release haploid ( uninucleate ) zoospores . These zoospores migrate in soil water for a limited distance (50 mm or less) to arrive at epidermal cells of meristematic tissues of growing points, buds, stolon tips, or young leaf primordia . Zoospores are short-lived and must encyst and infect susceptible host tissue within 1-2 hr after their formation. After infection by zoospores, potato host cells enlarge and haploid sori form inside the host cells while neighboring host cells begin to proliferate, resulting in the characteristic warty galls and the increased presence of the meristematic tissue that provides new infection courts for the fungus.
Each sorus contains one to nine summer sporangia, which in turn germinate to produce new haploid zoospores which reinfect susceptible tissue (i.e., a secondary disease cycle). These rapidly repeating secondary disease cycles ultimately result in an extensive invasion of host cells and rapid onset of gall formation. Young galls are a nutrient sink and expand rapidly at the expense of other plant tissue. For example, gall volume has been observed to increase more than 1,800-fold in 16 days
S pread and Survival Spread in soil by zoospores is limited (50 mm or less) to the infection zones of the plant. Soil water can carry zoospores downstream, although the lifespan of a released zoospore is 1-2 hours. Earthworms can move resting spores short distances. Wind is an active dispersal agent in regions of strong dry summer winds . Local dispersal has been shown in resting spores in soil attached to vehicles and contaminated manure. Long-range dispersal by tuber-movement, especially in international trade, attached soil and plants presents problems of control. The disease is essentially social, dependent on commercial crop and soil movement.
F avorable conditions The most favorable conditions for its development are warm temperatures (but not over 20 °C) with enough humidity. Winter sporangia can remain viable for up to 20–30 years. It can survive at depths of 50 cm in the soil. Three different fungi have been observed to parasitize the resting sporangia.
Integrated Disease Management (IDM) According to OEPP/EPPO (1990) specific quarantine requirement, potatoes should derive from a stock free of S.endobioticum . Use a continuous "cover crop" to reduce movement of inoculum via wind-blown soil. Amendment of infested soil with crushed crab shell (23% chitin) has been found to suppress the disease in some situations. Scheduling. Steam sterilization of soil. Soil treatment – mercuric chloride and formalin New tolerant or resistant varieties ( eg : Kufri Kanchar , Kufri sherpa , Kufri jyothi
References http://www.apsnet.org/publications/apsnetfeatures/pages/potatowart.aspx https://www.plantwise.org/KnowledgeBank/Datasheet.aspx?dsid=52315 R.S Singh, Plant disease, 9 th Edition, oxford IBH Publication Co-Pvt. Ltd Newdelhi , page no: 463 Ashok Aggarwal , R. S Mehrotra , P lant Pathology 3 rd edition, MC Graw Hill edu , Pvt. Ltd Chennai Page no: 541