Ralstonia solanacearum

Plant hosts that R. solanacearum infects include:

Crops

• Potato (Solanum tuberosum); tomato (Lycopersicum esculentum);[7] 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); rose (Rosa); and soybean (Glycine max).[8]

Wild hosts

• Woody nightshade (Solanum dulcamara)

Geranium:[9]

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

Potato:[9]

• Wilting of the leaves occurs at the end of the day with recovery at night. Plants eventually fail to recover and die.
• Brown staining of vascular ring happens and 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.

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]

Ralstonia solanacearum causes wilting at high populations (10⁸ – 10¹⁰ cfu/g tissue) and disperses in several routes. The large number of R. solanacearum can shed from roots of symptomatic and nonsymptomatic plants. Besides 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 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. The race 3 biovar 2 strain can survive in perennial nightshades which act as secondary hosts, and can also cause bacterial wilt of tomato.[10] Some EU states and Middle Eastern countries have not yet been able to eradicate this pathogen.

Ralstonia solanacearum usually enters the plant by a wound. Natural wounds (created by abscission of flowers, genesis of lateral roots) and unnatural ones (by agricultural practices or nematodes and xylem-feeding insects) could become entry sites for R. solanacearum. The bacteria get access to the wounds partially by flagellar-mediated swimming motility and chemotaxic attraction toward root exudates. Unlike many phytopathogenic bacteria, R. 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 systemically 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 xylem 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 bacterial populations in the xylem and is partially due to vascular dysfunction in which sufficient water cannot reach the leaves. 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 tissue in fully wilted plant. Ralstonia's systemic toxin also causes loss of stomatal control, but no evidence shows 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 weight EPS1. High bacterial densities are byproducts of plant cell wall degradation; tyloses and gums produced by the plant itself are other contributing factors to wilting.[1]

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 established, a strategy of integrated disease management is the best method 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 no completely immune cultivars are now available. Finally, a good rotation system that follows susceptible crops with resistant or nonhost 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.[18]

Wilting and yellowing of the leaves, as well as overall stunting of the plant, are typical symptoms.[21] The leaves may also take on a bronze cast[22] along with stems becoming streaked and tuber eyes becoming discolored. Tubers also start to rot if left in the ground. A milky-white sticky exudate or ooze, consisting of bacterial cells and their extracellular polysaccharide, is usually noticeable in freshly cut-sections of infected tubers.[23] Control of R. solanacearum is difficult because it is a soil borne pathogen, has wide host range, long survival in the soil, and has wide biological variation. No single control method has been found to be 100% effective, although in locations where the pathogen is established, some level of bacterial wilt control has been possible through use of a combination of diverse methods.[23] These methods include phytosanitation and cultural practices, chemical control, biological control, and host resistance. General sanitation practices are recommended to prevent spread of the disease, as chemical control is ineffective. Crop rotation with resistant crops is useful, as is altering the pH of the soil to keep it low in the summer (4-5), and higher in the fall (6.)[22]

Younger leaves of the plant will become flaccid, and adventitious roots may appear on the stem of the plant. The vascular system exhibits a progressively darker brown color as the disease progresses, in addition to possible lesions on the stem.[24] Management practices are similar to those of potato.

Typically, yellowing and wilting of older leaves occurs, as well as reduced fruit size and eventual rotting of the fruit.[25] In addition, flowers can become blackened and shriveled, and the vascular tissue discolored.[26] 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.[26]