Streptomyces ipomoea

Prepared by Emma Lookabaugh

Class Project for PP 728, Soilborne Plant Pathogens, Fall 2012


Streptomyces ipomoea

Host range and distribution:

Sweet potatoes; Ipomoea batatas; found in all major sweet potato production regions in the U.S. and Japan.


Streptomyces soil rot or pox is a widespread disease of sweet potato in North Carolina that results in a reduction in plant growth and severe yield losses. It is caused by the soilborne filamentous bacterium, Steptomyces ipomoea, and is able to persist in soil for many years in the absence of sweet potatoes. Fibrous roots and storage roots are infected in the field and symptom development varies based on the timing of root infection (Figure 1). Disease is favored by dry soils with pH above 5.2.

Two closely related Streptomyces species, Streptomyces scabies and Streptomyces acidiscabies, cause common scab of potato, beets, and radishes. Species of Streptomyces are well known for their ability to produce secondary metabolites. The common antibiotic, streptomycin, is produced by members in this genus.

Figure 1: Varied storage root symptoms of soil rot (Photo: Charles Averre, NCSU)


Streptomyces ipomoea is difficult to isolate and grows slowly in culture. Storage root lesions are often contaminated with secondary organisms. S. ipomoea is most easily isolated from infected fibrous roots early in the growing season. Select root pieces from the transition zone between black lesions and healthy root tissue. Surface sterilize in a 10% bleach solution or in a 0.525-1.05% hypochlorite solution for 2-5 minutes. Rinse with sterile deionized water and blot dry. Grind root tissue in a drop of sterile deionized water and streak onto Clark and Lawrence growth media (1). Incubate plates at 30C for several days. Monitor plates for colonies producing characteristic blue aerial mycelium. Transfer tentative colonies to slices of sterile storage roots for identification based on their ability to produce necrotic lesions.


S. ipomea is gram-positive, aerobic, heterotrophic, and strongly oxidative. S. ipomea produces spores in short, spiraled, chains. On some media, the spores may be compressed into balls. Individual spores are oval, about 1 m amd 1-2 m long, with smooth walls (Figure 2). Young colonies are usually white and smooth. As colonies age, aerial mycelium is produced. Initially white, the aerial mycelium turns a distinctive blue and becomes fuzzy in appearance (Figure 3). A method for rapid diagnosis has been developed using ELISA (3).

Figure 2: Scanning electron micrograph of a spiral spore chain of Streptomyces ipomoea.  Individual spores are approximately 1 m in diameter and 1-2 m long (Photo: Amanda Lawrence and C. A. Clark)

Figure 3: S. ipomoea growing on potato dextrose agar (left) on which it generally produces bald colonies without aerial mycelium, and on S. ipomoea growth medium (right) showing colonies with white aerial mycelium that has turned greenish blue as spore chains differentiated.  (Photo: C. A. Clark)


Symptom types vary based on timing of infection with respect to root development and cultivar. The primary symptom on fibrous roots is the formation of black, necrotic lesions followed by rot of the root tips (Figure 4). Lesions on storage roots are typically sunken (Figure 5). As lesions age, they turn dark brown to black and tissue becomes crusty (Figure 6). Cracking radiating out from the center can be observed in some lesions. Infections prior to root enlargement result in constriction near the point of infection, giving the root a distinct dumbbell shape (Figure 7). Lesions do not develop further during post-harvest storage.

Figure 4: Black rotted lesions on fibrous roots (Photo: Charles Averre, NCSU)

Figure 5: Sunken lesions on storage root (Photo: Clemson Univ. Slide Collection)

Figure 6: Black crusty lesions on storage roots (Photo: Charles Averre, NCSU)

Figure 7: Constricted storage root due to early infection by S. ipomoea (Photo: Charles Averre, NCSU)

Ecology and life cycle:

S. ipomoea is soilborne and persists in the soil for many years even in the absence of a sweet potato host. The primary host is sweet potato, but S. ipomoea has been shown to infect several weeds in the morning glory family. The importance of morning glory in the disease cycle is still unknown. S. ipomoea infects fibrous roots by direct penetration without the formation of appressoria or other specialized penetration structures. S. ipomoea is not able to directly infect mature storage roots. Lesions on storage roots are the result of fibrous root infection prior to enlargement or the pathogen entering through wounds. Spiral chains of spores are believed to be the primary overwintering structure.

Soil rot disease development is favored by dry soils with pH above 5.2. Soil rot is more severe where sweet potatoes are grown continuously in the same field. The pathogen is spread by the movement of infested soil, infected transplants and storage roots, and by contaminated equipment. Spread by wind or water erosion is possible. Disease does not normally spread in storage.


Effective management requires integrated control measures. Select fields with no history of soil rot. Avoid introducing S.ipomoea into fields by using only certified disease-free storage roots for propagation. Do not move equipment and machinery from infested fields to new fields. Consider using resistant varieties. Resistant and moderately resistant varieties include Bienville, Beauregard, Jasper, and Hernandez. Porto Rico and Jewel varieties are particularly susceptible to disease. Disease development is favored at high pH. Have field soil tested regularly and select fields with pH 5.2 or lower. Develop long-range crop rotation (3-4 years) in infested fields. Treat soil with a broad spectrum soil fumigant containing chloropicrin 2-4 weeks prior to planting. See The Grower Guide for recommended rates.

Links to other sites:

The Grower Guide

Sweet Potato Disease Management Chart

Selected references:

1.       Clark, C. A., and Lawrence, A. 1981. Morphology of spore-bearing structures in Streptomyces ipomoea. Canadian Journal of Microbiology 27: 575-579.

2.       Clark, C. A., and Matthews, S. W. 1987. Histopathology of sweet potato root infection by Streptomyces ipomoea. Phytopathology 77: 1418-1423.

3.       Moyer, J. W., and Echandi, E.1986. Serological detection and identification of Streptomyces ipomoea. Plant disease 70: 516-518.

4.       Labeda, D. P., and Lyons, A. J. 1992. DNA relatedness among strains of the sweet potato pathogen Streptomyces ipomoea (Person and Martin 1940) Waksman and Henrici 1948. Applied and environmental microbiology 58: 532-535.

5.   Clark, C.A., and Moyer, J.W. 1988. Compendium of Sweet Potato Diseases. APS Press. pp 6-8.