Ralstonia solanacearum

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Ralstonia solanacearum
Ralstonia solanacearum symptoms.jpg
Symptoms caused by Ralstonia solanacearum on tomato
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Beta Proteobacteria
Order: Burkholderiales
Family: Ralstoniaceae
Genus: Ralstonia
Binomial name
Ralstonia solanacearum
(Smith 1896)
Yabuuchi et al. 1996
Type strain
ATCC 11696

CCUG 14272
CFBP 2047
DSM 9544
ICMP 5712
JCM 10489
LMG 2299
NCAIM B.01459
NRRL B-3212


Burkholderia solanacearum (Smith 1896) Yabuuchi et al. 1993
Bacillus solanacearum Smith 1896
Pseudomonas solanacearum (Smith 1896) Smith 1914 Pseudomonas batatae Cheng and Faan 1962
Pseudomonas ricini (Archibald) Robbs 1954

Ralstonia solanacearum is an aerobic non-sporing, Gram-negative plant pathogenic bacterium. R. solanacearum is soil-borne and motile with a polar flagellar tuft. It colonises the xylem, causing bacterial wilt in a very wide range of potential host plants. It is known as Granville wilt when it occurs in tobacco. Bacterial wilts of tomato, pepper, eggplant and Irish potato caused by Ralstonia solanacearum were among the first diseases that Erwin Frink Smith proved to be caused by a bacterial pathogen. Because of its devastating lethality, R. solanacearum is now of the more intensively studied phytopathogenic bacteria and bacterial wilt of tomato is a model system for investigating mechanisms of pathogenesis.[1] Ralstonia was recently classified as Pseudomonas with similarity in most aspects, except that it does not produce fluorescent pigment like Pseudomonas.[2] The genome of R. solanacearum Strain GMI1000 has been sequenced.[3] Within the R. solanacearum species complex, there are four major monophyletic clusters of strains, termed phylotypes, that are geographically distinct: phylotypes I-IV are found in Asia, America, Africa, and Oceania, respectively.[1]

R. solanacearum was once considered as a possible biological control of Kahili Ginger (Hedychium gardnerianum), which is a member of '100 of the World's Worst Invasive Alien Species' in 2004.[4] However, R. solanacearum is no longer used as a biological control for Kahili Ginger in Hawaiian forests because of its wide host range. The ginger strain infects numerous ginger species, including edible ginger (Zingiber officinale), shampoo ginger (Zingiber zerumbet, pink ginger (Alpinia purpurata) and red ginger (Alpinia purpurata).[5]

Hosts and Symptoms[edit]

Photo of tomato plant with Ralstonia wilt symptoms
Photograph of tomato plant with Ralstonia wilt symptoms. Clemson University - USDA Cooperative Extension Slide Series


Plant hosts that R. solanacearum infects includes:

Crops: Potato (Solanum tuberosum); Tomato (Lycopersicum esculentum); Aubergine (egg plant) (Solanum melongena); Banana, (Musa spp); Geranium (common name) (Pelargonium); Ginger (Zingiber officinale); Tobacco (Nicotiana tabacum); Sweet pepper (Capsicum spp); Olive (Olea europea).

Wild hosts: Woody nightshade (Solanum dulcamara)


Geranium:[6] Wilting begins with lower leaves and petioles and works its way up the plant. Wilted leaves with chlorotic, wedge-shaped areas or chlorotic and/or necrotic leaf margins. No leaf spots are evident. Eventually entire plant collapses on the medium White runny ooze from cut stems

Potato:[6] Wilting of the leaves at the end of the day with recovery at night. Plant will eventually fail to recover and die. Brown staining of vascular ring. Pus may exude from the ring when the tuber is squeezed. Pale ooze may exude from eyes and heel end of potato. Soil will adhere to the oozing eyes. Cross-section of a stem placed in water will exude milky white strands. Unlike the fungal wilts, the leaves remains green in bacterial wilt.

Disease Cycle[edit]


Ralstonia solanacearum can overwinter in plant debris or diseased plants, wild hosts, seeds or vegetative propagative organs like tubers. The bacteria can survive for a long time in water (up to 40 years at 20–25 °C in pure water) and the bacterial population is reduced in extreme conditions (temperature, pH, salts, e.g.). Infected land sometimes cannot be used again for susceptible crops for several years.. R. solanacearum can also survive in cool weather and enter a state of being viable but not culturable. In most cases, this stage is not an agricultural threat because the bacteria usually become avirulent after recovering.[1]


R. solanacearum causes wilting at high population (108 – 1010 cfu/g tissue) and disperses in several routes. The large number of R. solanacearum can shed from roots of symptomatic and non-symptomatic plants. Beside that, bacterial ooze (which is usually used as a sign for detection)on plant surfaces, can enter the surrounding soil or water, contaminating farming equipment or may be acquired by insect vectors.[1] In addition, this pathogen can be spread out by contaminated flood water, irrigation, contaminated tools or infected seeds. In northern Europe, the pathogen has become established in solanaceous weeds which grow in slow moving rivers. When such contaminated water is used to irrigate potatoes, the pathogen enters the potato production system. Some EU states and Middle Eastern countries have not yet been able to eradicate this pathogen.


R. solanacearum usually enter the plant via a wound. Natural wounds (created by excision of flowers, genesis of lateral roots) as well as unnatural ones (by agricultural practices or nematodes and xylem-feeding bugs attack) would become entry sites for Ralstonia solanacearum. The bacteria get access to the wounds partially by flagellar-mediated swimming motility and chemotaxic attraction toward root exudates. Unlike many phytopathogenic bacteria, Ralstonia solanacearum potentially requires only one entry site to establish a systemic infection that results in bacterial wilt.[1]

After invading a susceptible host, R. solanacearum multiplies and moves systematically within the plant before bacterial wilt symptoms occur (Wilting should be considered as the most visible side effect that usually occurs after extensive colonization of the pathogen). When the pathogen gets into the xylems through natural openings or wounds, tyloses may form to block the axial migration of bacteria within the plant. In susceptible plants, this sometimes happens slowly and infrequently to prevent pathogen migration, and may instead lead to vascular dysfunction by unspecifically obstructing uncolonized vessels.

Wilting occurs at high level of bacterial population in the xylem and is partially due to vascular dysfunction in which water cannot reach the leaves sufficiently. At this time, extracellular polysaccharide (EPS1) content is about 10 μg/g tissue in the taproot, hypocotyl and midstem; EPS1 concentration is higher later on at more than 100 μg/g tissuein fully wilted plant. Wilting is due to vascular dysfunction that prevent water from reaching the leaves. Ralstonia's systemic toxin also causes loss of stomatal control but there is no evidence for excessive transpiration as its consequence. The primary factor contributing to wilting is probably blocking of pit membranes in the petioles and leaves by the high molecular mass EPS1. High bacterial densities, byproducts of plant cell wall degradation; tyloses and gums produced by the plant itself are other contributing factors to wilting.[1]

Virulence Mechanisms[edit]

R. solanacearum possesses genes for all six protein secretion pathways that have been characterized in Gram-negative bacteria. Perhaps the best-studied of these is the Type III secretion system (T3SS or TTSS), which secretes infection-promoting effector proteins (T3Es) into host cells. Approximately 74 suspected or confirmed T3Es have been identified in R. solanacearum to date, although the functions of very few are currently known. Despite being just one of several protein secretion systems, the T3SS is necessary for R. solanacearum to cause disease.[7] No single effector protein has been found to significantly alter pathogenicity of R. solanacearum, but simultaneous disruption of certain subsets of effectors (such as the set of seven GALA effectors in strain GMI1000) strongly affects virulence of the pathogen. GALA 7 is necessary for virulence on Medicago truncatula, hinting that T3E diversity may play a role in determining the broad host range of the R. solanacearum species complex.[8]

The Type III secretion system is not unique to R. solanacearum and is, in fact, very ancient. The evolutionary history of the T3SS is contested; a high degree of similarity to the flagellum has sparked debate over the relationship between these two structures.[1]

Approximately half of T3SS proteins are highly conserved in R. solanacearum and likely constitute a very old and stabilized effector core.[9] Among the other half showing variation among different strains of R. solanacearum, only a third show evidence of lateral gene transfer. The origins of the remaining effectors are unknown, although some researchers hypothesize that gene-for-gene interactions may play a significant role in shaping virulence genes in R. solanacearum.[10][11] Some of these effector proteins are homologous to Transcription Activator-like effectors (TAL effectors) from Xanthomonas [12] and could possibly have a similar function of activating specific genes in the host plant cells during R. solanacearum pathogenesis.


The environment that Ralstonia solanacearum is commonly found in is affected by the particular race (a genetically diverse population within a species), and the particular biovar (a strain that differs physiologically or biochemically from other strains.) Race 1, race 2 biovar 1, and race 3 biovar 2 are three of the most common and important strains of Ralstonia solanacearum. Race 1 strains have a broad host range including tobacco and bananas, and are usually found in tropical and subtropical environments as they have trouble surviving cooler temperatures, and are endemic to the southeastern United States.[13] Race 2 strains have a more limited host range than race 1, and are mostly restricted to tropical environments. Race 3 strains are more cold tolerant than the other two and are found in tropical highlands and temperate areas.[13] The host range for race 3 biovar 2 includes potatoes, tomatoes, and geraniums. Race 3 biovar 2 is very common throughout the world, but is not generally reported in North America,[14] and is therefore the focus of many sanitation and quarantine management practices to prevent the introduction or spread of the pathogen.


General Management[edit]

Commercial chemicals have generally proven to be ineffective in controlling the pathogen and are not recommended as a means of control.[1] In regions where the pathogen is endemic a strategy of integrated disease management (IDM) is the best strategy to reduce any impact of the pathogen. Using pathogen-free planting materials is a necessity. Planting resistant cultivars minimizes the ill effects of the pathogen, although there are currently no completely immune cultivars available. Finally, a good rotation system that follows susceptible crops with resistant or non-host crops can assist in diminishing the pathogen.[1] The pathogen is listed as a Select Agent in the United States; if the pathogen is detected by a proper authority a number of management protocols may be implemented. These can range from surveys to quarantines of infected and potentially infected plant material, which in turn may lead to larger eradication and sanitation programs.[13]

Specific Host Plant Symptoms and Management[edit]


Wilting and yellowing of the leaves as well as overall stunting of the plant are typical symptoms.[15] The leaves may also take on a bronze cast[16] along with stems becoming streaked and tuber eyes becoming discolored. Tubers will also start to rot if left in the ground. General sanitation practices are recommended to prevent spread of the disease as chemical control is ineffective. Crop rotation with resistant crops is useful as well as altering the pH of the soil keeping it low in the summer (4-5), and higher in the fall (6.)[16]


Younger leaves of the plant will become flaccid, and adventitious roots may appear on the stem of the plant. The vascular system will exhibit a progressively darker brown color as the disease progresses, in addition to possible lesions on the stem.[17] Management practices are similar for those of potato.


Typically yellowing and wilting of older leaves, as well as reduced fruit size and eventual rotting of the fruit.[18] In addition flowers can become blackened and shriveled, and the vascular tissue discolored.[19] Exclusion of the disease where it is not present is the only effective means of control. If an area does become infected all of the infected plants must be eliminated, which is why strong sanitation practices must be used to reduce the spread of disease.[19]


Ralstonia solanacearum is classified as one of the world's most important phytopathogenic bacteria due to its lethality, persistence, wide host range and broad geographic distribution. Although the pathogen causes major yield lost in the tropics and subtropics, it is currently a continuing threat in temperate climates.[1]

Ralstonia solanacearum is a high profile alien plant pathogen of A2 Quarantine status affecting a very wide range of crops. This means that it is present in parts of Europe but is under statutory control. Worldwide, the most important crops affected are: Potato, Tomato, Tobacco, Banana and Geranium. In the UK and the rest of the EU the most important crops affected are Potato and Tomato. It would cause serious economic damage were it to become more established than it currently is. Losses are due to actual yield reduction and also due to statutary measures taken to eliminate the disease.

Bacterial wilt caused by R. solanacearum is of economic importance because it infects over 250 plant species in over 50 families. It causes a wilt disease in several important agricultural crops such as potato, tomato, tobacco, banana, pepper and eggplant. The disease is known as Southern wilt, bacterial wilt, and brown rot of potato. Many more dicots suffer from the disease than do monocots. Among the monocot host, the order Zingiberales dominates with 5 over 9 families being infected by this bacterium.[1] The reason why some families are more susceptible to bacterial wilt is still unknown. Originally, Ralstonia solanacearum is found in tropical, sub-tropical and warm temperate climates, but is not believed to survive cold temperatures. However, this pathogen has recently been detected in geraniums (Pelargonium spp.) in Wisconsin, USA [20] and was traced back to the import of geranium cuttings to North America and Europe from the highland tropics where race 3 biovar 2 is endemic [21]

Brown rot of potato caused by Ralstonia solanacearum race 3 biovar 2 is among the most serious disease of potato worldwide, which is responsible for an estimated $950 million in losses each year.[22] Race 3 biovar 2 is cold tolerant and classified as a quarantine pathogen.[21] In addition, this race/biovar has been listed as a Select Agent in the Agriculture Bioterrorism Act of 2002 and is considered to have potential to be developed as a bioterrorist weapon.[20]


  1. ^ a b c d e f g h i j k Denny T., "Plant Pathogenic Ralstonia species" in GNANAMANICKAM, S. S. (2006). Plant-associated bacteria. Dordrecht, Springer. pp 1-62
  2. ^ Agrios, G. N. (2008). Plant pathology. Amsterdam [u.a.], Elsevier Academic Press, pp 647-649
  3. ^ "Ralstonia solanacearum". Bioinfo.genopole-toulouse.prd.fr. Retrieved 2012-09-24. 
  4. ^ Andersona R. C. and Gardner D. E. 1999. An Evaluation of the Wilt-Causing Bacterium Ralstonia solanacearum as a Potential Biological Control Agent for the Alien Kahili Ginger (Hedychium gardnerianum) in Hawaiian Forests. Biological Control 15 (2): 89-96
  5. ^ Paret, M.L., de Silva, A.S., Criley, R.A. and Alvarez, A.M. 2008. Ralstonia solanacearum Race 4:Risk Assessment for Edible Ginger. HortTechnology 18:90-96.
  6. ^ a b "Bacterial Wilt- Ralstonia solanacearum race 3 biovar 2". Massnrc.org. 2008-02-25. Retrieved 2012-09-24. 
  7. ^ Vasse, J; Genin, S.; Pascal, F.; Boucher, C.; Brito, B. (2000). "The hrpB and hrpG Regulatory Genes of Ralstonia solanacearum Are Required for Different Stages of the Tomato Root Infection Process". Molecular Plant-Microbe interactions 13 (3): 259–267. 
  8. ^ Angot, Aurelie; Peeters, N; Lechner, E; Vailleu, F; Baud, C; Gentzbittel, L; Sartorel, E; Genschik, P; Boucher, C; Genin, Stephane (2006). "Ralstonia solanacearum requires F-box-like domain-containing type III effectors to promote disease on several host plants". Proceedings of the National Academy of Sciences 103 (39): 14620–14625. doi:10.1073/pnas.0509393103. 
  9. ^ Remenant, Benoit; Coupat-Goutaland, B.; Guidot, A.; Cellier, G.; Prior, P. (2010). "Genomes of three tomato pathogens within the Ralstonia solanacearum species complex reveal significant evolutionary divergence". BMC Genomics 11 (1): 379. doi:10.1186/1471-2164-11-379. PMC 2900269. PMID 20550686. 
  10. ^ Poueymiro, M. and S. Genin. 2009. Secreted proteins from Ralstonia solanacearum: a hundred tricks to kill a plant. Current Opinion in Microbiology. 12: 44-52.
  11. ^ Genin, S. and C. Boucher. 2004. Lessons learned from the genome analysis of Ralstonia solanacearum. Annual Review of Phytopathology 42:107-134.
  12. ^ Heuer, H.; Yin, Y. -N.; Xue, Q. -Y.; Smalla, K.; Guo, J. -H. (2007). "Repeat Domain Diversity of avrBs3-Like Genes in Ralstonia solanacearum Strains and Association with Host Preferences in the Field". Applied and Environmental Microbiology 73 (13): 4379–4384. doi:10.1128/AEM.00367-07. PMC 1932761. PMID 17468277. 
  13. ^ a b c "R. solanacearum/Bacterial wilt - Brown rot of potato". Plantpath.ifas.ufl.edu. 2008-09-12. Retrieved 2012-09-24. 
  14. ^ http://www.aphis.usda.gov/plant_health/plant_pest_info/ralstonia/downloads/rasltoniaactionplanv4web.pdf
  15. ^ "Potato brown rot symptoms". Cals.ncsu.edu. Retrieved 2012-09-24. 
  16. ^ a b http://www.aphis.usda.gov/plant_health/plant_pest_info/ralstonia/downloads/ralstoniadatasheet_CPHST.pdf
  17. ^ "Tomato bacterial wilt symptoms". Cals.ncsu.edu. Retrieved 2012-09-24. 
  18. ^ "Banana Moko disease symptoms". Cals.ncsu.edu. Retrieved 2012-09-24. 
  19. ^ a b http://www.agric.wa.gov.au/objtwr/imported_assets/content/pw/ph/dis/fn/fs2006_moko_neyres.pdf
  20. ^ a b Hudelson B. 2005. University of Wisconsin Pest Alert - Ralstonia wilt.
  21. ^ a b Milling A., Meng F., Denny T., Allen C. 2009. Interactions with hosts at cool temperatures, not cold tolerance, explain the unique epidemiology of Ralstonia solanacearum race 3 biovar 2
  22. ^ Ephinstone, J. G. 2005. The current bacterial wilt situation: a global overview. pp 9-28 in: Bacterial Wilt: The Disease and the Ralstonia solanacearum Species Complex. C. Allen, P. Prior, and A. C. Hayward, eds. American Phytopathological Society, St. Paul, MN.

External links[edit]