Chlorotic symptoms

Pares and co-workers (1992) showed that the cucumber mosaic virus (CMV) was present in leaves showing mosaic, mottled, and chlorotic symptoms. Subsequently, Davis and colleagues (1996) found that CMV was widely distributed in kava plants in all major kava-producing countries. They also showed that the symptoms of the dieback disease developed on plants inoculated with CMV, usually within three to four weeks after leaf symptoms first became visible. It is now accepted that the CMV is the main causative agent for the kava dieback disease. The disease is also aggravated by plant-sucking pests such as the leaf miner and aphids which create entry in the cells for the CMV, and by infections from soil borne nematodes, fungi, and bacteria. 

Used pre- and postemergence, dichlormate kills young sensitive seedlings. After treatment, sensitive weeds show on sprouting extreme chlorotic symptoms and wither because of the inhibition of chlorophyll synthesis. 

The development of toxic symptoms caused by urea herbicides depends on the particular herbicide, on the species of the plant and the application rate. Generally, the action of urea herbicides is not rapid, though after the application of higher doses chlorotic symptoms develop within a few days in sensitive plants such as beans. The death of the plants usually occurs within weeks. 

It is translocated relatively slowly from the leaves to the roots and tubers. Depending on temperature, light intensity and air and soil moisture, translocation proceeds in 4-8 days, the effect being manifested by chlorotic symptoms, which develop in 2-4 weeks into necrosis. Combined with other translocatable herbicides, such as 2,4-D, 2,4-DB or silvex, basipetal translocation and thus herbicidal action can be increased, and regrowth from tubers reduced. 

Photosynthesis in plants can be inhibited by many conditions, such as invasion by viral pathogens. The effects of TMV on photosynthesis are quite variable (4-6), which may reflect the different effects on photosynthesis induced by the different TMV strains. One of the key issues still to be resolved with the pathology of viral infection is what viral effect causes the expression of disease symptoms. Since TMV infection can affect leaf development and pigmentation and often plant growth, it is quite likely that a primal site of TMV infection is in the chloroplast. However, it is not known if the expression of chlorotic symptoms from TMV infection is the result of the inhibition of photosynthesis (5,7,8) or if TMV inhibits some other host process which induces symptoms and this then causes the inhibition of photosynthesis. 

In monocotyledonous plants (grasses and cereals) and some others, there is no division of mesophyll tissue, and injury normally appears as a bifacial fleck.Some plants, after extended exposure to low concentrations of pollution (either continuously or intermittently), produce chlorotic patterns that may be distinctive of oxidant pollution or similar to symptoms of normal senescence. The early senescence seen in some plants may be a result of long-term exposure to ambient oxidants. 

Differential susceptibility of individual clones of eastern white pine to ozone and sulfur dioxide was shown by Berry and Heggestad and Costonis. When Dochinger et a/. determined that chlorotic dwarf could be caused by an interaction of ozone and sulfur dioxide, th used a chlorotic dwarf-susceptible clone to eliminate the genotype variable. Houston tested the response of tolerant and susceptible clones of eastern white pine (on the basis of symptom expression under ambient conditions) to ozone or sulfur dioxide. Injury caused by sulfur dioxide or sulfur dioxide plus ozone correlated well with the earlier field responses, but ozone did not produce a consistent response. They also found that a 6-h exposure to a mixture of sulfur dioxide and ozone caused a difference in needle elongation between clones within tolerant and sensitive groups. This suggests that tolerance may function over a wide range of responses. 

Injury to important primary-producer species constituting forest ecosystems is not limited to California. In the eastern United States, a disease called emergence tipbum of eastern white pine was related to ozone by Berry and Ripperton. Occurrence of similar symptoms on the same species in eastern Canada could not be definitely related to ozone by Linzon.- The disease is characterized by bands of necrosis initiated in the semimature tissue of elongating needles the necrosis spreads to the needle tip. In other studies with ozone fumigations at 0.07 ppm for 4 h or 0.03 ppm for 48 h, the tipbum appeared additional symptoms were silvery or chlorotic flecks and chlorotic mottling. - ... 

A recent review of the metabolites of L. maculans and L biglobosa produced in diverse culture conditions [19] emphasized that both species biosynthesize host-selective and non-selective phytotoxins. Importantly, it was shown that the composition of metabolite profiles of L. maculans depended on the composition of the culture medium. In a chemically defined liquid medium, isolates virulent on canola produced mainly sirodesmin PL (1), a non-host-selective phytotoxin, minor sirodesmins with one, three, or four sulfurs bridging the dioxopiperazine ring (sirodesmin H (3) [20], sirodesmin J (4) and K (5) [21]) and phomalirazine (6) (Fig. 9.1). The various sirodesmins 1-5 and phomalirazine (6) caused necrotic lesions of different intensities on leaves of both resistant and susceptible plants. Phomalide (7), the first host-selective phytotoxin isolated from virulent isolates of L. maculans, caused disease symptoms (necrotic, chlorotic, and reddish lesions) on canola (susceptible to L maculans) but not on brown mustard or white mustard... 

L. maculans isolates Laird 2 and Mayfair 2 (virulent on brown mustard but not on canola) produced in a chemically defined medium the host-selective phytotoxin depsilairdin (8) (Fig. 9.2), containing a novel amino acid residue ((25,35,45)-3,4-dihydroxy-3-methylprolyl) and a sesquiterpene moiety (lairdinol A, synthesized recently [25,26]). Depsilairdin (8) caused disease symptoms similar to those caused by the pathogen on brown mustard, that is, strong necrotic and chlorotic lesions, but no lesions on canola. 

When the EBI fungicides are applied later than 72-96 hours after the beginning of the scab infection period but before symptoms are visible, chlorotic spots or flecks with few or no conidia are produced in place of typical sporulating lesions (Figure 2). This is referred to as presymptom control by Szkolnik (23) and it is a form of post-infection or curative action. Dodine and benomyl are examples of fungicides with presymptom activity. Presymptom activity becomes more obvious as the time of application increases beyond the 72-96 hour after-infection period. In greenhouse trials, sprays of bltertanol, etaconazole, fenarimol and triforine reduced conidial production 85 to 99% when applied five days after inoculation (20). 

Lead is considered to be a non-essential metal to plants, and only a small proportion of the lead in soils is biovailable to plants (Alloway, 1990). Visible symptoms of toxicity, though unspecific to Pb, are smaller leaves and a stunted growth. Leaves may become chlorotic and reddish with necrosis and the roots may turn black. Several plant species, ecotypes and bacterial strains have been known to develop Pb tolerance. The phytotoxicity of Pb is low as it has very limited availability and uptake from soil and soil solutions. However, plant roots are usually able to take up and accumulate large quantities of Pb2+ in soil and culture solutions but translocation to aerial shoots is generally limited due to binding at root surfaces and cell walls (Lagerwerff, 1971 Jones et al., 1973 Lane and Martin, 1977). 

Diseases of plants may arise from attack by fungi, bacteria, viruses, insects or parasitic plants. Insects may also act as the vectors of plant diseases and provide routes for pathogens to enter plants. The disease may be manifest by decayed or swollen roots, shrivelled or lost fruit, chlorotic or wilting leaves, necrotic lesions on the stems, leaves or fruit, excessive gum formation or the formation of cankers. In this chapter we are eoncerned with the chemistry of the fungal attack on plants that lead to these symptoms. 

Bacterial leaf spots is a disease affecting lettuce plants caused by Xanthomonas campestris pv. vitians, recently reclassified as X. hortorum pv. vitians [74]. This disease does not normally produce severe losses [75], but outbreaks occur during periods of heavy rainfall [76]. The leaves of infected plants show translucent, water-soaked brown lesions that become dark with age. These types of symptoms, and the fact that the bacterium is generally not isolated from the chlorotic halos surrounding the dead tissues, suggest the involvement of toxic compounds in the disease developments. Two phytotoxic metabolites were isolated from the culture filtrates of X h. pv. vitians, which were identified as 3-methylthiopropanoic and -methylthiopropenoic... 

Specific symptoms of sodium excess are not known. High levels of sodium reduced calcium uptake in some cases (Leh 1973). Citrus and stone fruit species are particularly susceptible to salt damage. The leaf damage sometimes starts with chlorotic blotches, which are followed by necrotic lesions at the leaf tips and margins or between the veins. The leaves of lucerne growing on saline soils turn reddish, and the leafstalks collapse, possibly indicating calcium deficiency (Bergmann 1992). 

Appearance of white, yellow or orange chlorotic spots or stripes on older leaves, usually starting from leaf tips and margins. In some species, irregularly distributed chlorotic spots appear, but in all cases symptoms start from the leaf tip. The base of the leaf usually remains dark green. 

Wallace et al. (1977), in describing symptoms of titanium toxicity, reported that chlorotic and necrotic spots occurred on the leaves of bush beans containing about 200 mg Ti kg DM. Titanium levels in plants range from 0.15 to 6.5 mgkg DM, and some species of plants, including horsetail Equisetum sp.) and nettle Urtica sp.), as well as certain diatoms, can accumulate much higher levels of the element (Kabata-Pendias 2000). Various titanium compounds were shown not to be mutagenic in Bacillus subtilis (Nordman and Berlin 1986). 

One-three days after the herbicide is applied the first symptoms become visible, depending on weed species and climatic conditions. Chlorotic spots and necrotic zones increase rapidly. These symptoms develop either simultaneously as in most dicot weeds or subsequently as in grasses. In grasses intensive chlorosis usually precedes wilting and desiccation. Usually, the treated plants are killed within 7-10 days. Low temperatures delay the herbicidal activity significantly. Sublethal doses or unfavorable climatic conditions may lead to regrowth, especially on older plants. 

Chlorotic and necrotic spots in the interveinal areas of leaves are symptoms of manganese deficiency in plants (42). In tomato leaves, the chloropasts are the first part of the plant to be affected (43). 

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