Beet vascular necrosis
Beet vascular necrosis | |
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Scientific classification | |
Domain: | Bacteria |
Phylum: | Pseudomonadota |
Class: | Gammaproteobacteria |
Order: | Enterobacterales |
Family: | Pectobacteriaceae |
Genus: | Pectobacterium |
Species: | |
Subspecies: | P. c. subsp. betavasculorum
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Trinomial name | |
Pectobacterium carotovorum subsp. betavasculorum (Thomson et al. 1984) Hauben et al. 1999
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Synonyms | |
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Beet vascular necrosis and rot is a soft rot disease caused by the bacterium Pectobacterium carotovorum subsp. betavasculorum, which has also been known as Pectobacterium betavasculorum and Erwinia carotovora subsp. betavasculorum.
Hosts
Fodder beets,
Breeding for resistance to other diseases such as beet yellows virus without also selecting for vascular necrosis resistance can leave cultivars susceptible to the pathogen. For example, the use of USH9A and H9B in California’s San Joaquin valley is thought to have led to an epiphytotic (severe) outbreak of disease in the early 1970s.[8] This was likely because of the limited gene pool used when selecting strongly for resistance to beet yellows virus. Further information on resistant cultivars can be found in the section Management.[citation needed]
In addition to beets, Pectobacterium carotovara subsp. betavasculorum can also infect tomato, potato, carrots, sweet potato, radish, sunflower, artichokes, squash, cucumber and chrysanthemum.
Symptoms
Symptoms can be found on both beet roots and foliage, although foliar symptoms are not always present. If present, foliar symptoms include dark streaking along petioles and viscous froth deposits on the crown which are a by-product of bacterial metabolism.[12] Petioles can also become necrotic and demonstrate vascular necrosis. When roots become severely affected, wilting also occurs.[1] Below ground symptoms include both soft and dry root rot. Affected vascular bundles in roots become necrotic and brown, and tissue adjacent to necrosis becomes pink upon air contact.[1] The plants that do not die completely may have rotted-out, cavernous roots.[citation needed]
Various pathogens can cause root rot in beets; however the black streaking on petioles and necrotic vascular bundles in roots and adjacent pink tissue help to distinguish this disease from others such as Fusarium Yellows. Additionally, sampling from the rhizosphere of infected plants and serological tests can confirm the presence of Erwinia caratovora subs.[11]
Disease cycle
Pectobacterium carotovorum subsp. betavasculorum is a
Upon death of the sugar beet, or harvest of the field, the pathogen appears to survive in select living plant tissue like beet roots,[4] or volunteer beets.[6] However, it does not appear to survive in sugar beet seeds,[4][5][6] or live in the soil after harvest.[4][5] It is also possible for the pathogen to infect injured carrots, potato, sweet potato, tomato, radish, sunflower, artichokes, squash, cucumber and chrysanthemums;[4][6][9] however, since those are often planted in the same season as sugar beets, they are not likely to be overwintering hosts.
Environment
Injury to the leaves, petioles or crown is mandatory for the pathogen to gain entry to the host tissue.[4][6] Accordingly, hail damage is correlated with a higher degree of disease outbreak.[4] Young plants (less than eight weeks old) are also considered to be more prone to infection[4][6]
Temperature and availability of moisture are key factors in determining the rate of disease development. Warm temperatures, 25-30 °C, promote rapid disease development.,[4][6][14] and can result in acute symptoms.[4] Symptoms are also reported to appear at temperatures as low as 18 °C, but disease development is slowed;[5] below that temperature, infections do not develop.[4] Excessive water also promotes disease development by providing a more optimal environment for the pathogen,[14] and has been shown to be a key factor in augmenting disease outbreak in fields with sprinkler irrigation[4]
Agricultural
The degree of
The spacing between plants also impacts the degree of infection: greater in-row spacing results in more diseased roots.[15] This may be due to the fact that greater spacing promotes faster growth, and hence greater probability of cracks in the crown,[6] or because of the increased amount of nitrogen available per plant.[4]
Since the pathogen has multiple hosts, it is important for farmers to be wary of other plants in the surrounding area. It is possible for the pathogen to survive in weedy hosts, and can infect injured carrots, potato, sweet potato, tomato, radish, squash, and cucumber.[6][9][14] Hence, the presence of these plants may increase the supply of inoculum.
Laboratory
If the pathogen is cultured in a lab, it can grow on Miller and Schroth media, can use sucrose to make reducing sugars, and can use either lactose, methyl alpha-glucoside, inulin or raffinose to make acids.[4] It is also capable of surviving in culture medium sodium levels of up to 7–9%,[4] and in temperatures as high as 39 °C.[16]
Management
Since the bacteria cannot survive in seeds,
Cultural practices
Because the bacteria readily enter the plant through wounds, management practices that decrease injury to the plants are important to control the spread of the disease.[17] Cultivation is not recommended, as the machinery can become contaminated and physically spread the bacteria around the soil. Accidental leaf tearing or root scarring can also occur depending on the size of the crop, allowing the bacteria to enter more individual plants. If hilling the beets, great care must be taken to avoid getting soil into the crown,[18] because the pathogen is soil-borne and this could expose the plant to more bacteria, thus increasing the risk of infection.[citation needed]
While most bacteria are motile and can swim, they cannot move very far due to their small size. However, they can be carried along by water, and a significant movement of Pectobacterium can be attributed to being carried downstream from irrigation and rainwater.[3] To control the spread of the disease, limiting irrigation is another strategy. The bacteria also flourishes in wet conditions, so limiting excess water can control both the spread and severity of the disease.[citation needed]
Increased in-row spacing also causes more severe disease. In an infected field, yield decreased linearly when spacing was greater than 15 cm (6 in),[15] so a spacing of 6 inches or less is recommended.
The bacteria can also utilize nitrogen fertilizer to accelerate their growth, thus limiting or eliminating the amount of nitrogen fertilizer applied will lessen the disease severity.[14] For example, when fertilizer was applied to an infected field the infection rate per root increased from 11% (with no added nitrogen) to 36% (with 336 kg nitrogen/hectare), and sugar yields decreased.[15]
Cultivar | Resistance | Source |
---|---|---|
H9 | No | [15] |
H10 | No | |
C17 | No | |
546 H3 | Moderate | |
C13 | No | [19] |
E540 | No | |
E538 | No | |
E534 | Moderate | |
E502 | Moderate | |
E506 | Yes | |
E536 | Yes | |
C930-35 | Moderate | [20] |
C927-4 | Moderate | |
C930-19 | Yes | |
C929-62 | Yes |
Resistance
The bacteria can survive in the rhizosphere of other crops such as tomato, carrots, sweet potato, radish, and squash[1][4] as well as weed plants like lupin and pigweed,[11] so it is very hard to get rid of it completely.[3] When it is known that the bacterium is present in the soil, planting resistant varieties can be the best defense against the disease. Many available beet cultivars are resistant to Pectobacterium carotovorum subsp. betavasculorum, and some examples are provided in the corresponding table. A comprehensive list is maintained by the USDA on the Germplasm Resources Information Network.[21] Even though some genes associated with root defense response have been identified, the specific mechanism of resistance is unknown, and it is currently being researched.[22]
Biological control
Some
While it is more difficult to apply bacteriophages in a field setting, it is not impossible, and laboratory and greenhouse trials are showing bacteriophages to potentially be a very effective control mechanism. However, there are a few obstacles to surmount before field trials can begin.
Importance
The disease was first identified in the western states of, California, Washington, Texas, Arizona and Idaho in the 1970s and initially led to substantial yield losses in those areas.[15] Erwinia caratovara subsp betavascularum was not discovered in Montana until 1998. When it first appeared, beet vascular necrosis caused individual farm yield loss ranging from 5–70% in Montana's Bighorn Valley.[7] Today, yield losses from the disease are generally infrequent and patchy as most producers plant resistant varieties. Infection rate is generally low if resistant cultivars are chosen; however, warmer and wetter conditions can lead to higher than normal instance of disease[7]
If infection does occur, bacterial root rots can not only cause economic losses in the field, but also can in storage and processing as well.[12] In processing plants, rotten roots complicate slicing and the bacterially-produced slime can clog filters. This is especially problematic with late-infected beets which are generally harvested and processed along with healthy beets. The disease can also lower sugar-content which greatly reduces the quality[8]
References
- ^ a b c d e f Whitney, E.D, ed. (1986). Compendium of Beet Diseases and Insects (2nd ed.). St. Paul, MN: American Phytopathological Society.
- ^ Dye, DW (1969). "A taxonomic study of the genus Erwinia. II. The "carotovora" group". New Zealand Journal of Science. 12: 81–97.
- ^ .
- ^ a b c d e f g h i j k l m n o p q r s t u v Haverson, R.M., ed. (2009). Compendium of Beet Diseases and Pests (2nd ed.). St. Paul, MN: American Phytopathological Society. pp. 58–59.
- ^ . Retrieved 17 October 2013.
- ^ a b c d e f g h i j k l m "Sugar Beet Production Guide, Chapter 11: Disease Management, pg 138-139" (PDF). University of Nebraska – Lincoln Extension, 2013. Archived from the original (PDF) on 27 June 2010. Retrieved 17 October 2013.
- ^ . Retrieved 18 October 2013.
- ^ S2CID 53705630.
- ^ .
- ^ De Boer, Solke H. (2004). "Blackleg of Potato". The Plant Health Instructor. Retrieved 17 October 2013.
- ^ .
- ^ PMID 30769681.
- PMID 21469936.
- ^ a b c d e "Sugar Beet (Beta vulgaris)-Bacterial Vascular Necrosis and Rot {Erwinia Root Rot}". pacific northwest plant disease management handbook. Retrieved 17 October 2013.
- ^ . Retrieved 17 October 2013.
- ]
- ^ Gallian, John J. "Management of Sugarbeet Root Rots" (PDF). Pacific Northwest Extension. Retrieved 17 October 2013.
- ^ "UC Pest Management Guidelines". University of California Agriculture and Natural Resources. Retrieved 17 October 2013.
- . Retrieved 17 October 2013.
- . Retrieved 17 October 2013.
- ^ "Germplasm Resources Information Network". United States Department of Agriculture. Archived from the original on 23 September 2015. Retrieved 28 September 2013.
- ^ Smigocki, A C. "Molecular Approaches To Pest And Pathogen Resistance in Sugar Beet". united states department of agriculture agricultural research service. Retrieved 17 October 2013.
- ^ Duffy, B (2006). "Biological control of bacterial diseases in field crops". Symposium on Biological Control of Bacterial Plant Diseases: 93–98. Archived from the original on 5 July 2015. Retrieved 17 October 2013.
- ^ S2CID 85123748.
- S2CID 30527360.
- PMID 22934116.
- PMID 23531902. Archived from the originalon 24 December 2013. Retrieved 17 October 2013.
- PMID 20214607.