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UC Pest Management Guidelines


Silver scurf

Potato

Silver Scurf

Pathogen: Helminthosporium solani

(Reviewed 1/08, updated 5/08)

In this Guideline:


SYMPTOMS AND SIGNS

Symptoms of silver scurf usually appear on the stem end of tubers as small light brown or grayish leathery spots and may enlarge to cover most of the tuber surface. Lesions have a shiny appearance that is more pronounced when tubers are wet. Margins of young lesions are frequently dark brown and sooty from spore production. Microscopic examination reveals tiny "Christmastree-like" spore structures formed by the production of conidiophores with conidia (spores) attached.

Black dot tuber lesions have a similar appearance but do not have dark, sooty margins and usually contain numerous tiny black dots (sclerotia) that have small microscopic spines. The two diseases can be present on the same tuber. Silver scurf is most noticeable on red‑skinned and other smooth-skinned cultivars but can cause substantial damage on russet cultivars. Smooth skin cultivars can be severely infected and rendered unsalable at harvest whereas all cultivars can be substantially damaged during storage. Affected tubers are more susceptible to decay and shrinkage from water loss during storage.

COMMENTS ON THE DISEASE

The fungus that causes silver scurf, Helminthosporium solani, survives on infected seed tubers and on plant debris in infested soil. Spores are produced in lesions that develop on infected seed pieces and spread the disease to daughter tubers. New tubers also can be infected by spores present in infested soil.

Helminthosporium solani infects tubers through lenticels or directly through the skin and remains confined to the periderm and outer layers of cortex cells. The incidence and severity of the disease increase over time if tubers are left in infested soil. Once tubers are placed into storage, silver scurf lesions can continue to develop, and secondary spread of the disease to other tubes in storage can continue when temperatures are above 37°F and humidity is above 90%. Disease incidence increases the longer tubers are held in storage. With time, all tubers within a storage can be severely infected by this pathogen.

If early generation seed tubers are held in common storage with later-generation seed tubers, silver scurf may spread to the early generation from the later generation, which is more likely to have some disease present. Likewise, if multiple lots of potatoes are placed into common storage, a lot infected with silver scurf will produce spores that move through the air system, infecting other lots.

MANAGEMENT

To minimize silver scurf, plant certified seed tubers free of the disease and use seed treatments known to be effective against the silver scurf pathogen. Seed can be assayed before planting to assess silver scurf levels. Harvest as soon as tubers have matured after vinekill. Daughter tubers can also be assayed for silver scurf to help determine risk of damage in storage and determine which lots should be used first. Use humidified airflow to remove free moisture from wet tubers as quickly as possible, and keep storage temperatures as low as possible. The silver scurf pathogen does not survive long periods in the soil so practice a normal crop rotation practice of 2 or more years out of potatoes.

Thoroughly clean and disinfect storages before storing a new crop. Do not store early generation seed tubers in the same storage as later-generation seed tubers. Do not repeatedly enter storages over a long period of time and do not begin to remove tubers without completely emptying the storage. Activity in storages encourages the release of spores into the air system and increases levels of silver scurf, particularly if new infections are given enough time to develop. The use of chemicals in the air system of storages has not been proven to reduce losses to silver scurf.

PUBLICATION

[UC Peer Reviewed]

UC IPM Pest Management Guidelines: Potato
UC ANR Publication 3463
Diseases
R. M. Davis, Plant Pathology, UC Davis
J. Nuñez, UC Cooperative Extension, Kern Co.
B. J. Aegerter, UC Cooperative Extension, San Joaquin Co.
Acknowledgment for contributions to the disease section:
C. Smart, Plant Pathology, UC Davis

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