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Nutrient Disorders




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Fig. 1. Hedera helix with marginal burn
caused by excess fertilizer.
(Click image for
expanded view).


Some of the most common abiotic diseases are due to nutritional imbalances resulting from applications of insufficient or excessive amounts of macronutrients or micronutrients (Fig. 1). Plants need greater quantities of macronutrients than micronutrients, but some of the most dramatic symptoms of nutritional imbalance are caused by deficiencies or toxicities of micronutrients such as boron, copper, and fluoride. Soilless growing media, water alkalinity, and unbalanced nutritional programs all contribute to the problem. It can be difficult to recognize symptoms of nutrient disorders because they are often subtle or not unique to the cause. Also, different cultivars may vary widely in their susceptibility to deficiencies or toxicities.

Deficiencies

Nutrient deficiencies cause chronic disease in plants. When nutrients are lacking, important molecules like chlorophyll, DNA, RNA, proteins, and lipids cannot be manufactured. Enzymes may not carry out important chemical transformat­ions. In general, plant growth is slowed, and susceptibility to disease may increase. Flowering potted plants may be dwarfed, develop chlorosis or necrosis, have fewer flowers, and otherwise be unattractive.


Fig. 2. Typical symptoms of fertilizer deficiency in an unfertilized Aphelandra squarrosa. From the Compendium of Ornamental Foliage Plant Diseases.

Nitrogen is easily leached and must be supplied to plants frequently to prevent deficiency. A general chlorosis of the entire surface of older leaves, progressing upwards, is the most common symptom of nitrogen deficiency. Leaves may be reduced in size, internodes are shortened, and eventually a general loss of vigor or growth occurs (Fig. 2).

Phosphorus. One of the first symptoms of phosphorus deficiency is the production of small leaves and shortened internodes. Older leaves may lose their shine and become dull and eventually chlorotic. Green pigments are lost, so that red, yellow, and blue pigments show through, especially near main veins on the underside of leaves.

Potassium. Leaf and stem size are often reduced in plants that are deficient in potassium. The foliage remains its normal color on some plants; on others, necrosis and chlorosis occur, developing first on older leaves (Fig. 3).


Fig. 3. Older leaf of potassium-deficient Dictyosperma album. From Diseases and Disorders of Ornamental Palms.

Magnesium. A general reduction in plant vigor and reduced leaf size are common symptoms of magnesium deficiency. Interveinal and marginal chlorosis and necrosis also occur, developing first on older leaves (Fig. 4). On Philodendron scandens C. Koch & H. Sello subsp. oxycardium (Schott) Bunt. (heart-leaf philodendron), chlorosis occurs in a marginal V-shaped pattern. On some palms, only the tip becomes chlorotic. The chlorosis is a bronze color, and veins remain dark green. Premature senescence of older leaves may occur in mild cases.


Fig. 4. Magnesium deficiency
on Phoenix. (Click image for
expanded view). 

Calcium deficiency is not common in foliage or flowering plants. Small yellow lesions form on the basal half of older leaves of calcium-deficient plants. Water-soaked spots often develop within the chlorotic areas. Symptoms progress into younger leaves, and the chlorotic spots become necrotic, so that leaves sometimes abscise prematurely. Color breaks occur on spathe tissue of calcium-deficient Anthurium andraeanum Linden (Andrae’s flamingo flower). Internodes of Ficus benjamina L. (weeping fig) become elongated and weak, and its leaves become chlorotic and stunted. Some cultivars of poinsettia (Euphorbia pulcherrima Willd. ex Klotzsch), such as Gutbier V-14 Glory and Celebrate II, develop bract necrosis when foliar tissue calcium levels are low, a condition that is difficult to distinguish from bract necrosis caused by Botrytis.


Fig. 5. New leaf of iron-deficient Caryota mitis. (Click image for expanded view). 

Iron can become deficient under interiorscape conditions and when the pH of the growing medium is above 7. However, the occurrence of iron defi­ciency is largely dependent on the specific requirements of the plant. Chlorosis of the youngest leaves, often with the veins remaining green, is the most common symptom of iron deficiency (Fig. 5). Yellowing, stunting, and abscission of new leaves can also occur. Soil pH can influence the availability of iron to plants and should be monitored periodically. The ability of roots to absorb iron is reduced by poor root health caused by inadequate soil aeration resulting from excess soil water.

Sulfur deficiency is rare under normal conditions of plant production. An overall chlorosis of new leaves occurs. This symptom is easily confused with the chlorosis caused by nitrogen deficiency in some plants.

Manganese deficiency occurs in some plants such as large palms with deformation and chlorosis of newly emerging leaves as the most obvious symptom. Plants that completely lack manganese can be severely stunted.

Boron deficient plants have shortened internodes, thickened stems, and reduced leaf size. New leaves of deficient Ficus elastica Roxb. Ex Hornem. (India-rubber tree) are stunted and deformed and become brittle and stiff. Terminal leaves are especially distorted.

Copper deficiency causes severe distortion and stunting of new growth. One of the most common examples of this deficiency occurs in Aglaonema commutatum Schott ‘Fransher.’ It’s leaves are distorted and dwarfed and sometimes have a hooked appearance, with the edges rolled upward toward the center (Fig. 6). Terminal buds die, and laterals sometimes initiate growth, forming a witches’-broom.


Fig. 6. Copper deficiency on Aglaonema. (Click image for expanded view).

Zinc deficiency has been identified in only one foliage plant, Chrysalidocarpus lutescens H. Wendl. (areca palm). Leaves of all ages become uniformly chlorotic and terminal leaves are triangular, stunted, and deformed.

Molybdenum is needed in small amounts by plants, but the use of soilless media and fertilizers lacking this element can result in deficiencies in poinsettia. Symptoms are similar to those of nitrogen or iron deficiency and ammonium toxicity. Plants may be stunted, leaves are small and chlorotic, and leaf margins may become scorched. Leaves tend to curl upward.

Toxicities

Excessive levels of nutrients may be toxic to some plants. Symptoms are usually marginal or tip chlorosis and necrosis (Fig. 1). Chlorosis of lower leaves occurs in some cases. Plants may die as a result of overfertilization. Root systems of over fertilized plants are reduced and may appear to be infected with a root pathogen or parasite.


Fig. 7. Wilting of florist's geranium caused by root injury from an excessive level of soluble salts in the growing mix. (Click image for expanded view).

Soluble salts is the most common example of toxicity. This occurs when too high a concentration of fertilizer salts is present in the soil solution. Soluble salts toxicity is usually evidenced by chlorosis or necrosis of the leaf margins that begins with the lower leaves. In some plants, leaves become dark green and growth may be stunted. In severe cases, wilt or defoliation may occur (Fig. 7). Plants vary in their tolerance to high salt levels, and their stage of growth can also be important. Soluble salts are readily leached from the growing medium.



The macronutrient elements
(nitrogen, phosphorus, potassium, sulfur, calcium, and magnesium) are generally not toxic in high amounts. However, high levels of calcium or potassium may interfere with root uptake of magnesium. Foliar calcium levels of 2.9% were reported to result in a significant reduction in total bract area of poinsettia. Excessive rates of nitrogen may result in an increase in susceptibility to bacterial soft rot and other diseases.


Fig. 8. Ammonium toxicity on schefflera. From Foliage Plant Diseases: Diagnosis and Control.

Ammonium. Excessive levels of ammonium (NH4) in the growing medium may interfere with the uptake of calcium, but more commonly, ammonium is directly toxic to plants. Excessive levels can cause reduced growth, interveinal chlorosis, foliar marginal chlorosis or necrosis, and damage to the root system (Fig. 8). Fertilizer programs should provide no more than one-half the total nitrogen in the ammonium and/or urea form for flowering potted plants. Ammonium toxicity may occur when fertilizers containing urea or ammonium sulfate are used. Excessive levels of ammonium may also occur after steaming of organic soils, especially those containing manure. The conversion of ammo­nium to nitrate is carried out by soil microorganisms that are nonexistent or in low numbers in soilless growing media. The conversion can be inhibited by certain pesticides; cool, wet soil; low pH; excessive soluble salts; and poor aeration. Fertilizers containing significant levels of ammonium should be avoided when a soilless medium is used. Ammonium is difficult to leach from the growing medium.

Micronutrients are generally toxic when present in high amounts. In particular, boron, manganese, aluminum, and iron can cause various problems to plants. Plants can vary con­siderably from cultivar to cultivar in their susceptibility to nutrient toxicities. The pH of the growing medium can significantly affect plant uptake of micronutrients.



Fig. 9. Manganese toxicity on pothos. (Click image for expanded view).

Manganese and iron toxicity is relatively common in greenhouse crops when the pH of the soil is low and additional micronutrients are being added to the crop from fertilizer sources. Steaming soil may also release manganese into the soil solution. When foliar levels of manganese and iron are high, the upper leaves become chlorotic, especially at the margins. Small dots of necrosis may occur scattered on the margins of lower leaves (Fig. 9). Chlorosis is also common. Margins may become necrotic. Some geranium cultivars (Pelargonium spp.) develop leaf-edge burn and necrotic flecking when grown at a pH of less than 6.0.



Fig. 10. Boron toxicity on Aglaonema 'Maria.' From Foliage Plant Diseases: Diagnosis and Control.

Boron toxicity has been identified in several foliage plants, including Aglaonema commutatum Schott, cultivars of Ficus elastica Roxb. Ex Hornem. (Indian-rubber tree), and Chlorophytum comosum (Thunb.) Jacques (spider plant). Symptoms on India-rubber tree are small necrotic lesions with chlorotic halos on the underside of leaves, often clustered around leaf margins. Boron toxicity in A. communtatum ‘Maria' causes greasy-looking marginal lesions (Fig. 10), which are easily confused with symptoms of bacterial leaf diseases and virtually indistinguishable from symptoms of fluoride toxicity of this plant. In contrast, boron and fluoride toxicity of spider plant can be distinguished by lesion color and by the demarcation between healthy and necrotic tissues. Boron toxicity causes tipburn with an indistinct, grayish margin between healthy and necrotic tissue, whereas fluoride toxicity causes lesions with a more distinct, purplish red margin bordering the necrotic tissue. Applications of boron to sensitive plants should be avoided.

Copper toxicity occurs in several species of palms. Elongated, reddish brown lesions form on young leaves (Fig. 11). Excesses of other micronutrients also cause the same symptoms, which in addition are difficult to distinguish from fungal leaf spots of these plants. Micronutrient toxicity can occur in palms treated with micronutrient sprays or fungicides and bactericides containing copper or iron, even at labeled rates and intervals. Applications of these products should be avoided when plants are small.


Fig. 11. Copper toxicity on Chamaedorea. From Foliage Plant Diseases: Diagnosis and Control.

Iron toxicity occurs in Chrysalidocarpus lutescens H. Wendl. (areca palm) sprayed with either an iron sequestrant or fungicides containing iron, such as ferbam. The symptoms are similar to those caused by excess copper or by fungal leaf pathogens.


Fig. 12. Fluoride toxicity on Dracaena 'Warneckii.' From Foliage Plant Diseases: Diagnosis and Control.


Fig. 13. Fluoride-toxicity on Chrysalidocarpus lutescens. From Diseases and Disorders of Ornamental Palms.

Fluoride. The most common micronutrient toxicity is caused by excess fluoride. The list of sensitive plants is long (e.g., Table 29 in the Compendium of Ornamental Foliage Plant Diseases). Fluoride damage is characteristic for each plant under specific conditions. The first plant found sensitive to fluoride was Cordyline terminalis (L.) Kunth (ti plant). Its typical symptoms are marginal chlorosis and necrosis, which are especially prevalent during rooting. Most species of Dracaena are damaged by excess fluoride. Probably the most widely recognized fluoride damage on a foliage plant is that of D. deremensis Engl. ‘Warneckii,’ on which elliptical necrotic lesions, usually less than 1 cm long, form in chains in the white band of tissue (Fig. 12). D. fragrans (L.) Ker-Gawl, ‘Massageana’ (corn plant) can develop dramatic marginal necrosis or dark green ring spots or mottling. Chamaedorea elegans Mart. (parlor palm) and Chrysalidocarpus lutescens H. Wendl. (areca palm) are also sensitive to fluoride (Fig. 13). Foliar tipburn and necrotic lesions on pinnae are common on parlor palm subjected to excess fluoride. Elliptical, necrotic lesions form on areca palm, often in interveinal chains. Fluoride toxicity also occurs in some Calathea spp., typically causing chlorotic and necrotic lesions on leaf margins. Toxic levels of fluoride can be produced by various sources, including superphosphate fertilizer, perlite, water, and some peats. Fluoride damage on numerous crops has been effectively reduced by the addition of dolomite or calcium hydroxide to the potting medium to increase its pH and thereby reduce the solubility of fluoride. Sensitive plants should be grown in a potting medium of pH 6.0 or more.

Selected References

Ball, V., ed. 1991. Ball Red Book. 15th ed. George J. Ball, West Chicago, IL.

Biernbaum, J. A., Carlson, W. H., Schoemaker, C., and Heins, R. D. 1988. Low pH causes iron and manganese toxicity. Greenhouse Grower 6:92-97.

Bould, C., Hewitt, E. J., and Needham, P. 1983. Diagnosis of Mineral Disorders in Plants. Vol. 1, Principles. Her Majesty’s Stationery Office, London.

Cox, D. A. 1988. Lime, molybdenum, and cultivar effects on molyb­denum deficiency of poinsettia. J. Plant Nutr. 11:589-603.

Cox, D. A. 1992. Poinsettia cultivars differ in their response to molybdenum deficiency. HortScience 27:892-893.

Cox, D. A., and Seeley, J. G. 1980. Magnesium nutrition of poin­settia. HortScience 15:822-823.

Cox, D. A., and Seeley, J. G. 1984. Ammonium injury to poinsettia: Effects of NH4N:NO3-N ratio and pH control in solution culture on growth, N absorption, and N utilization. J. Am. Soc. Hortic. Sci. 109:57-62.

Engelhard, A. W., ed. 1989. Soilborne Plant Pathogens: Management of Diseases with Macro- and Microelements. American Phyto­pathological Society, St. Paul, MN.

Harbaugh, B. K., and Woltz, S. S. 1989. Fertilization practice and foliar-bract calcium sprays reduce incidence of marginal bract necrosis of poinsettia. HortScience 24:465-468.

Joiner, N. J., Poole, R. T., and Conover, C. A. 1983. Nutrition and fertilization of ornamental greenhouse crops. Hortic. Rev. 5:317-401.

Judd, L. K., and Cox, D. A. 1992. Growth of New Guinea impatiens inhibited by high growth-medium electrical conductivity. Hort­Science 27:1193-1194.

Knauss, J. F. 1986. The role of boron in plant nutrition. Grower Talks, Jan., pp. 106-108, 110, 112.

Mastalerz, J. 1977. The Greenhouse Environment. John Wiley & Sons, New York.

Winsor, G., and Adams, P. 1987. Diagnosis of Mineral Disorders in Plants. Vol. 3, Glasshouse Crops. Her Majesty’s Stationery Office, London.



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