Bacterial blight of soybean is a widespread disease of soybeans caused by Pseudomonas syringae pv. glycinea.
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Bacterial blight of soybean is a widespread disease of soybeans caused by Pseudomonas syringae pv. glycinea.
Soybeans are grown all over the world and are a primary source of vegetable oil and protein. [1] Approximately 40% of the world's supply of vegetable oil comes from soybeans. [1] Therefore, it is important to guarantee a successful soybean crop every growing season. Bacterial blight can be found in most soybean fields every year in the Midwest. [2] Yield losses due to Pseudomonas syringae pv. glycinea have been reported as anywhere from 4% to 40% depending on the severity of the conditions. [1] The disease does not normally affect yield levels as it occurs early in the growth of soybeans and the crop is able to compensate the loss of photosynthetic area. [3] It is still adventitious to monitor for bacterial blight as substantial loss may occur when susceptible cultivars are grown under unfavorable conditions. Pseudomonas syringae pv glycinea should be monitored carefully in seed production fields as it is seed borne and can affect seed quality. [2] A study conducted by Stefani et al. in 1998 found that seeds with contamination levels ranging from 0.5 to 20% did not lead to any significant yield loss when grown in warm and dry regions. [3] Usage of resistant cultivars in the proper environment is therefore an effective way of eliminating the impact of this pathogen. It is not uncommon for countries to have quarantines in place for this pathogen as the inoculum is often spread in soybean seeds. [3]
Bacterial blight of soybean is caused by the bacterial agent Pseudomonas syringae pv. glycinea. This bacterium also causes disease in snap bean (Phaseolus vulgaris) and lima bean (Phaseolus lunatus), however it is more commonly seen in soybean. [4] Pseudomonas syringae pv. glycinea attacks all of the above-ground parts of soybean, but symptoms are typically seen on the mid-upper canopy of leaves and pods. [5] After infection, small, water-soaked spots surrounded by a chlorotic halo appear on the leaves. The brown or black centers of these spots indicate that the tissue is dying. Typically these spots will enlarge and merge to form large, dead patches on the leaves. [6] The leaves appear ragged if the dead tissue falls out. Lesions on pods are initially small and water-soaked but eventually enlarge, turn brown to black, and merge to encompass the whole pod. [7] Infection can also occur on the stems, petioles and seeds. [6]
Pseudomonas syringae pv. glycinea overwinters in crop residue and in seeds. [8] Infection usually begins when the infected plant material is carried by a rainstorm with high winds to healthy soybean plants. [2] Bacteria can enter through natural openings (stomata) or through wounds. In order to enter through natural openings, however, water must be present on the leaf surface. [7] Bacterial Blight may appear after infected seedlings are planted and begin to emerge. In addition to being spread via wind and rain, transmission may occur when leaves of infected soybean rub against leaves of healthy soybean. Symptoms begin to appear 5–7 days after infection. [7]
Bacterial blight of soybeans can enter leaves through wounds or natural openings such as stomata. [9] After gaining entrance to the host leaves, Pseudomonas syringae pv. glycinea multiplies in the leaf intercellular fluid. [10] The pathogen must then overcome the plants defenses. Pseudomonas syringae pv. glycinea accomplishes this by using the type three secretion system to inject a variety of pathogenicity effector proteins (Hrp proteins) into the plant cell cytoplasm. [11] These proteins act by interfering with effector-triggered immunity and producing phytohormones/toxins that suppress plant defenses. [11] The expression of these virulence factors depends on the environmental conditions at the time of infection (see "environment section). [11] Furthermore, expression of virulence factors will only take place when a sufficiently large population of bacteria is present, which is determined through quorum sensing. [11] When successful, the common symptoms of bacterial blight will be seen, with the main effect on the plant being a reduction in photosynthetic leaf area. Generally, the amount of photosynthetic area lost is not enough to impede plant growth. [3] As the plant continues to grow it overcomes the loss of photosynthetic area and reduction in yield, if there is any, is negligible. [3]
A variety of phytotoxins that contribute to the severity of disease have been identified in Pseudomonas syringae. Coronatine has been identified in Pseudomonas syringae pv. glycinea, which is responsible for the development of chlorosis.[ citation needed ] Necrosis inducing phytotoxins include syringomycins and syringopeptins.[ citation needed ]
A complex relationship between hypersensitive response and pathogenicity genes, avirulence genes, and plant resistance genes gives rise to the virulence of bacterial pathogens. Generally, a single avirulence gene (in the bacterium) corresponds to a single resistance gene (in the plant host), giving rise to the concept of a gene-for-gene response. [12] The avirulence gene leads to the pathogen being avirulent, or unable to induce disease on a specific variety of plant hosts, those being the ones carrying the corresponding resistance genes. [12] Soybean cultivars that have been bread to contain resistance genes Rpg1, Rpg2, Rpg3, and Rpg4 have been shown to be resistant to Pseudomonas syringae pv. glycinea race 4. [13] The corresponding avirulence genes in the bacterium are avrB, avrA, avrC, and avrD. [13] A different race of Pseudomonas syringae pv. glycinea may still be able to elicit disease in these soybean cultivars as it may carry different avirulence genes. Researchers have shown that the exchange of avirulence genes can switch a race from being virulent to avirulent and vice versa. [14] Thus, evolution, mutation, and cases of horizontal gene transfer can make it difficult to breed longterm resistance into soybean cultivars.[ citation needed ]
Members of the family Pseudomonadaceae are highly resilient organisms. [15] They have been found in virtually every habitat in which they have been sought: from the deepest parts of the oceans to the soils of the highest mountains. [15] It thus comes as no surprise that Pseudomonas syringae pv. glycinea is able to adapt to a wide range of environmental conditions.[ citation needed ]
However, research suggests that moist conditions and temperatures between 23 and 28 °C provide optimal growing conditions for the pathogen. [6] [15]
Additionally, monocultures contribute to making the disease endemic by providing organic materials (crop residue) in which the pathogen may overwinter. [6]
Since bacterial blight of soybean can be transmitted via infected seeds, one of the most efficient control method is to use clean seeds. [6] Clean seeds are commercially available at any of the major seed retailers in the world (e.g. Monsanto). The advantage of getting seeds from industrial vendors is that the latter guarantee the lack of pathogenic activity in the seeds.[ citation needed ]
Crop rotation has also been shown to be effective in limiting both the spread and the severity of bacterial blight outbreaks in soybean fields. [6] Rotating crops limits the amount of both living and dead tissue that the pathogen can invade, and thereby limits the overall incidence of the disease in a given land area. Therefore, soybeans should be rotated with non-susceptible crops.[ citation needed ]
Avoiding susceptible soybean cultivars is yet another method commonly used amongst American farmers to avoid disease outbreaks. [8]
Successful chemical control can also be achieved by spraying a mixture of streptocycline and copper oxychloride on young plants, although this is an uncommon practice due to the higher cost of treatment. [1] However, in the recent years, scientists have discovered that leaf extracts from neem, ginger, garlic and onion also have the ability to significantly reduce the impact of bacterial blight in soybean. [1]
Plant pathology is the scientific study of diseases in plants caused by pathogens and environmental conditions. Organisms that cause infectious disease include fungi, oomycetes, bacteria, viruses, viroids, virus-like organisms, phytoplasmas, protozoa, nematodes and parasitic plants. Not included are ectoparasites like insects, mites, vertebrate, or other pests that affect plant health by eating plant tissues. Plant pathology also involves the study of pathogen identification, disease etiology, disease cycles, economic impact, plant disease epidemiology, plant disease resistance, how plant diseases affect humans and animals, pathosystem genetics, and management of plant diseases.
A leaf spot is a limited, discoloured, diseased area of a leaf that is caused by fungal, bacterial or viral plant diseases, or by injuries from nematodes, insects, environmental factors, toxicity or herbicides. These discoloured spots or lesions often have a centre of necrosis. Symptoms can overlap across causal agents, however differing signs and symptoms of certain pathogens can lead to the diagnosis of the type of leaf spot disease. Prolonged wet and humid conditions promote leaf spot disease and most pathogens are spread by wind, splashing rain or irrigation that carry the disease to other leaves.
Phytophthora sojae is an oomycete and a soil-borne plant pathogen that causes stem and root rot of soybean. This is a prevalent disease in most soybean growing regions, and a major cause of crop loss. In wet conditions the pathogen produces zoospores that move in water and are attracted to soybean roots. Zoospores can attach to roots, germinate, and infect the plant tissues. Diseased roots develop lesions that may spread up the stem and eventually kill the entire plant. Phytophthora sojae also produces oospores that can remain dormant in the soil over the winter, or longer, and germinate when conditions are favourable. Oospores may also be spread by animals or machinery.
The gene-for-gene relationship was discovered by Harold Henry Flor who was working with rust (Melampsora lini) of flax (Linum usitatissimum). Flor showed that the inheritance of both resistance in the host and parasite ability to cause disease is controlled by pairs of matching genes. One is a plant gene called the resistance (R) gene. The other is a parasite gene called the avirulence (Avr) gene. Plants producing a specific R gene product are resistant towards a pathogen that produces the corresponding Avr gene product. Gene-for-gene relationships are a widespread and very important aspect of plant disease resistance. Another example can be seen with Lactuca serriola versus Bremia lactucae.
Leptosphaeria maculans is a fungal pathogen of the phylum Ascomycota that is the causal agent of blackleg disease on Brassica crops. Its genome has been sequenced, and L. maculans is a well-studied model phytopathogenic fungus. Symptoms of blackleg generally include basal stem cankers, small grey lesions on leaves, and root rot. The major yield loss is due to stem canker. The fungus is dispersed by the wind as ascospores or rain splash in the case of the conidia. L. maculans grows best in wet conditions and a temperature range of 5–20 degrees Celsius. Rotation of crops, removal of stubble, application of fungicide, and crop resistance are all used to manage blackleg. The fungus is an important pathogen of Brassica napus (canola) crops.
Xanthomonas campestris is a gram-negative, obligate aerobic bacterium that is a member of the Xanthomonas genus, which is a group of bacteria that are commonly known for their association with plant disease. The species is considered to be dominant amongst its genus, as it originally had over 140 identified pathovars and has been found to infect both monocotyledonous and dicotyledonous plants of economical value with various plant diseases. This includes "black rot" in cruciferous vegetables, bacterial wilt of turfgrass, bacterial blight, and leaf spot, for example.
Pseudomonas syringae is a rod-shaped, Gram-negative bacterium with polar flagella. As a plant pathogen, it can infect a wide range of species, and exists as over 50 different pathovars, all of which are available to researchers from international culture collections such as the NCPPB, ICMP, and others.
Pseudomonas cichorii is a Gram-negative soil bacterium that is pathogenic to plants. It has a wide host range, and can have an important economical impact on lettuce, celery and chrysanthemum crops. P. cichorii was first isolated on endives, from which it derives its name. It produces 6-aminopenicillanic acid. Based on 16S rRNA analysis, P. cichorii has been placed in the P. syringae group.
Pseudomonas viridiflava is a fluorescent, Gram-negative, soil bacterium that is pathogenic to plants. It was originally isolated from the dwarf or runner bean, in Switzerland. Based on 16S rRNA analysis, P. viridiflava has been placed in the P. syringae group. Following ribotypical analysis misidentified strains of Pseudomonas syringae pv. ribicola and Pseudomonas syringae pv. primulae were incorporated into this species. This pathogen causes bacterial blight of Kiwifruit.
Pseudomonas amygdali is a Gram-negative plant pathogenic bacterium. It is named after its ability to cause disease on almond trees. Different analyses, including 16S rRNA analysis, DNA-DNA hybridization, and MLST clearly placed P. amygdali in the P. syringae group together with the species Pseudomonas ficuserectae and Pseudomonas meliae, and 27 pathovars of Pseudomonas syringae/Pseudomonas savastanoi, constituting a single, well-defined phylogenetic group which should be considered as a single species. This phylogenetic group has not been formally named because of the lack of reliable means to differentiate it phenotypically from closely related species, and it is currently known as either genomospecies 2 or phylogroup 3. When it is formally named, the correct name for this new species should be Pseudomonas amygdali, which takes precedence over all the other names of taxa from this group, including Pseudomonas savastanoi, which is and inadequate and confusing name whose use is not recommended.
Pseudomonas cannabina is a gray, Gram-negative, fluorescent, motile, flagellated, aerobic bacterium that causes leaf and stem rot of hemp, from which it derives its name. It was formerly classified as a pathovar of Pseudomonas syringae, but following ribotypical analysis, it was reinstated as a species. The type strain is CFBP 2341.
Ralstonia solanacearum is an aerobic non-spore-forming, 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 R. 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 one of the more intensively studied phytopathogenic bacteria, and bacterial wilt of tomato is a model system for investigating mechanisms of pathogenesis. Ralstonia was until recently classified as Pseudomonas, with similarity in most aspects, except that it does not produce fluorescent pigment like Pseudomonas. The genomes from different strains vary from 5.5 Mb up to 6 Mb, roughly being 3.5 Mb of a chromosome and 2 Mb of a megaplasmid. While the strain GMI1000 was one of the first phytopathogenic bacteria to have its genome completed, the strain UY031 was the first R. solanacearum to have its methylome reported. Within the R. solanacearum species complex, the four major monophyletic clusters of strains are termed phylotypes, that are geographically distinct: phylotypes I-IV are found in Asia, the Americas, Africa, and Oceania, respectively.
Xanthomonas is a genus of bacteria, many of which cause plant diseases. There are at least 27 plant associated Xanthomonas spp., that all together infect at least 400 plant species. Different species typically have specific host and/or tissue range and colonization strategies.
Halo blight of bean is a bacterial disease caused by Pseudomonas syringae pv. phaseolicola. Halo blight’s pathogen is a gram-negative, aerobic, polar-flagellated and non-spore forming bacteria. This bacterial disease was first discovered in the early 1920s, and rapidly became the major disease of beans throughout the world. The disease favors the places where temperatures are moderate and plentiful inoculum is available.
Cercospora sojina is a fungal plant pathogen which causes frogeye leaf spot of soybeans. Frog eye leaf spot is a major disease on soybeans in the southern U.S. and has recently started to expand into the northern U.S. where soybeans are grown. The disease is also found in other soybean production areas of the world.
Plant disease resistance protects plants from pathogens in two ways: by pre-formed structures and chemicals, and by infection-induced responses of the immune system. Relative to a susceptible plant, disease resistance is the reduction of pathogen growth on or in the plant, while the term disease tolerance describes plants that exhibit little disease damage despite substantial pathogen levels. Disease outcome is determined by the three-way interaction of the pathogen, the plant and the environmental conditions.
Xanthomonas axonopodis pv. manihotis is the pathogen that causes bacterial blight of cassava. Originally discovered in Brazil in 1912, the disease has followed the cultivation of cassava across the world. Among diseases which afflict cassava worldwide, bacterial blight causes the largest losses in terms of yield.
Xanthomonas oryzae pv. oryzae is a bacterial pathovar that causes a serious blight of rice, other grasses, and sedges.
Bacterial leaf streak (BLS), also known as black chaff, is a common bacterial disease of wheat. The disease is caused by the bacterial species Xanthomonas translucens pv. undulosa. The pathogen is found globally, but is a primary problem in the US in the lower mid-south and can reduce yields by up to 40 percent.[6] BLS is primarily seed-borne and survives in and on the seed, but may also survive in crop residue in the soil in the off-season. During the growing season, the bacteria may transfer from plant to plant by contact, but it is primarily spread by rain, wind and insect contact. The bacteria thrives in moist environments, and produces a cream to yellow bacterial ooze, which, when dry, appears light colored and scale-like, resulting in a streak on the leaves. The invasion of the head of wheat causes bands of necrotic tissue on the awns, which is called Black Chaff.[14] The disease is not easily managed, as there are no pesticides on the market for treatment of the infection. There are some resistant cultivars available, but no seed treatment exists. Some integrated pest management (IPM) techniques may be used to assist with preventing infection although, none will completely prevent the disease.[2]
Xanthomonas campestris pv. juglandis is an anaerobic, Gram negative, rod-shaped bacteria that can affect walnut trees though the flowers, buds, shoots, branches, trunk, and fruit. It can have devastating effects including premature fruit drop and lesions on the plant. This pathogen was first isolated by Newton B. Pierce in California in 1896 and was then named Pseudomonas juglandis. In 1905 it was reclassified as Bacterium juglandis, in 1930 it became Phytomas juglandis, and in 1939 it was named Xanthomas juglandis. The International Standards for Naming Pathovars declared it to be named Xanthomonas campestris pv. juglandis in 1980. There have been recent proposals to change the name once again to Xanthomonas arboricola pv. juglandis, but this has not yet been universally accepted.