Rhizoctonia diseases occur throughout the world.

They cause losses on almost all vegetables and flowers, several field crops, turfgrasses, and even perennial ornamentals, shrubs, and trees. Symptoms may vary somewhat on the different crops, with the stage of growth at which the plant becomes infected, and with the prevailing environmental conditions. The most common symptoms on most plants are damping-off of seedlings and root rot, stem rot, or stem canker of growing and grown plants (Fig. 11-151). On some hosts, however, Rhizoctonia also causes rotting of storage organs (Fig. 11-152) and foliage blights or spots (Fig. 11-153), especially of foliage near the ground. Damping-off is probably the most common symptom caused by Rhizoctonia on most plants it affects (Fig. 11151E). It occurs primarily in cold, wet soils. Very young seedlings may be killed before or soon after they emerge from the soil. Thick, fleshy seedlings such as those of legumes and the sprouts from potato tubers may show noticeable brown lesions and dead tips before they are killed. After the seedlings have emerged, the fungus attacks their stem and makes it water soaked, soft, and incapable of supporting the seedling, which then falls over and dies. In older seedlings, invasion of the fungus is limited to the outer cortical tissues, which develop elongate, tan to reddishbrown lesions. The lesions may increase in length and width until they finally girdle the stem, and the plant may die; alternatively, as often happens in crucifers, before the plant dies the stem turns brownish black and may be bent or twisted without breaking, giving the disease the name wire stem (Fig. 11-151A). A seedling stem canker, known as soreshin, is common and destructive in cotton, tobacco, and other seedlings that have escaped the damping-off or seedling blight phase of the disease. It develops under conditions that are not especially favorable to the disease. Soreshin lesions appear as reddish-brown, sunken cankers that range from narrow to completely girdling the stem near the soil line (Fig. 11-151). As soil temperature rises later in the season, affected plants may show partial recovery due to new root growth. Root lesions form in seedlings and on partly grown or mature plants. Reddish-brown lesions usually appear first just below the soil line, but in cool, wet weather the lesions enlarge in all directions and may increase in size and number to include the whole base of the plant and most of the roots. This results in weakening, yellowing, and sometimes death of the plant. On low-lying plants such as lettuce and cabbage, lower leaves touching the ground or close to it are attacked at the petioles and midribs. Reddish-brown, slightly sunken lesions develop and the entire leaf becomes dark brown and slimy. From the lower leaves the infection spreads upward to the next leaves until most or all leaves, and the head, may be invaded and rot, with mycelium and sclerotia permeating the tissues or nestled between the leaves. On lawn and turfgrasses, Rhizoctonia causes brown patch (Fig. 11-153C), a disease particularly severe during periods of hot and humid or wet weather, especially with heavy dew periods. Roughly circular areas appear, ranging from a few centimeters to one or more meters in diameter, in which the grass blades become water soaked and dark at first but soon become dry, wither, and turn light brown. Diseased areas appear slightly sunken; at the border of the diseased areas, where the fungus is still active and attacking new grass blades, however, infected leaves look water soaked and dark. On damp days or in the early morning hours the areas appear as a characteristic grayish black smoke ring 2 to 5 centimeters wide. As the grass dries, the activity of the fungus slows down or stops and the ring disappears. Brown to black, hard, round sclerotia about 2 millimeters in diameter form in the thatch, diseased plants, and soil. In brown patch, Rhizoctonia usually kills only the leaf blades, and plants in the affected area begin to recover and grow again from the center outward, resulting in a doughnut-shaped diseased area. On fleshy, succulent stems and roots and on tubers, bulbs, and corms, Rhizoctonia causes brown rotten areas that may be superficial or may extend inward to the middle of the root or stem. The rotting tissues usually decompose and dry, forming a sunken area filled with the dried plant parts mixed with fungus mycelium and sclerotia (Fig. 11152). On potato tubers, Rhizoctonia causes black scurf, in which small, hard, black sclerotia occur on the tuber surface and are not removed by washing (Fig. 11-152B), or russeting or russet scab, in which the skin becomes roughened in a criss-cross pattern resembling the shallow form of common potato scab. Finally, Rhizoctonia causes rots on fruits and pods lying on or near the soil, such as cucumbers (Fig. 11-152), tomatoes, eggplants, and beans. These rots develop most frequently in wet, cool weather and appear first in the field but may continue to spread to other fruits after harvest and during transportation and storage. In the sheath and culm blight of rice (Figs. 11-153A and 11-153B), one of the most serious diseases of rice and sometimes important on other cereals as well, different Rhizoctonia species cause large, irregular lesions that have a straw-colored center and a wide, reddishbrown margin. Seedlings and mature plants may become blighted under favorable conditions for the pathogen. The Pathogen. Rhizoctonia spp. represent a large, diverse, and complex group of fungi. All Rhizoctonia fungi exist primarily as sterile mycelium and, sometimes, as small sclerotia that show no internal tissue differentiation. Mycelial cells of the most important species, R. solani, contain several nuclei (multinucleate Rhizoctonia), whereas mycelial cells of several other species contain two nuclei (binucleate Rhizoctonia). The mycelium, which is colorless when young but turns yellowish or light brown with age, consists of long cells and produces branches that grow at approximately right angles to the main hypha, are slightly constricted at the junction, and have a cross wall near the junction (Fig. 11-153D). The branching characteristics are usually the only ones available for identification of the fungus as Rhizoctonia. Under certain conditions the fungus produces sclerotia-like tufts of short, broad cells that function as chlamydospores, or eventually the tufts develop into rather small, loosely formed brown to black sclerotia, which are common on some hosts such as potato. As mentioned earlier, Rhizoctonia species infrequently produce a basidiomycetous perfect stage. The perfect stage of the multinucleate R. solani is Thanatephorus cucumeris, whereas that of binucleate Rhizoctonia is Ceratobasidium. A few multinucleate Rhizoctonia spp. (R.

zeae and R. oryzae) have Waitea as their perfect basidiomycetous stage. The perfect stage forms under high humidity and appears as a thin, mildew-like growth on soil, leaves, and infected stems just above the ground line. Basidia are produced on a membranous layer of mycelium and have four sterigmata, each bearing one basidiospore. It has now become evident that Rhizoctonia solani and other species are collective species, consisting of several more or less unrelated strains. The Rhizoctonia strains are distinguished from one another because anastomosis (fusion of touching hyphae) occurs only between isolates of the same anastomosis group. After anastomosis, which can be detected microscopically, an occasional heterokaryon hypha may be produced, under certain conditions, from one of the anastomosing cells. In the vast majority of anastomoses, however, five to six cells on either side of the fusion cells become vacuolated and die, appearing as a clear zone at the junction of two colonies. This killing reaction between isolates of the same anastomosis group is the expression of somatic or vegetative incompatibility. Such somatic incompatibility limits outbreeding to a few compatible pairings. The existence of anastomosis groups in Rhizoctonia solani represents genetic isolation of the populations in each group. Although the various anastomosis groups are not entirely host specific, they show certain fairly well defined tendencies: isolates of anastomosis group 1 (AG1) cause seed and hypocotyl rot and aerial (sheath) and web blights of many plant species; isolates of AG2 cause canker of root crops, wire stem on crucifers, and brown patch on turfgrasses; isolates of AG3 affect mostly potato, causing stem cankers and stolon lesions and producing black sclerotia on tubers; and isolates of AG4 infect a wide variety of plant species, causing seed and hypocotyl rot on almost all angiosperms and stem lesions near the soil line on most legumes, cotton, and sugar beets. Six more anastomosis groups are known within R. solani and there are many more in other Rhizoctonia. Recognition of the existence of anastomosis groups and of their lesser or greater host specificity has been important in determining the anastomosis group of the isolate that must be used for inoculations in breeding different crops for resistance to Rhizoctonia and of the propagules counted for making disease predictions for the various crops affected by that fungus. Development of Disease. The pathogen overwinters usually as mycelium or sclerotia in the soil and in or on infected perennial plants or propagative material such as potato tubers. In some hosts the fungus may even be carried in the seed (Fig. 11-154). The fungus is present in most soils and, once established in a field, remains there indefinitely. The fungus spreads with rain, irrigation, or flood water; with tools and anything else that carries contaminated soil; and with infected or contaminated propagative materials. For most races of the fungus the optimum temperature for infection is about 15 to 18C, but some races are most active at much higher temperatures, up to 35C. Disease is more severe in soils that are moderately wet than in soils that are waterlogged or dry. Infection of young plants is most severe when plant growth is slow because of adverse environmental conditions for the plant. Control. Control of Rhizoctonia diseases is difficult. Wet, poorly drained areas should be avoided or drained better. Disease-free seeds should be planted on raised beds under conditions that encourage fast growth of the seedling. There should be wide spaces among plants for good aeration of the soil surface and of plants. When possible, as in greenhouses and seed beds, the soil should be sterilized with steam or treated with chemicals. Drenching of soil with pentachloronitrobenzene (PCNB) helps reduce damping-off in seed beds andgreenhouses. When specific races of the pathogen have built up, a 3-year crop rotation with another crop may be valuable. With most vegetables, no effective fungicides are available against Rhizoctonia diseases, although some other chemicals are sometimes recommended as soil drenches before planting and spraying them once or twice on the seedlings soon after emergence. On turfgrasses, fungicide applications with some contact and systemic fungicides seem to provide effective control. Since the mid-1980s, tremendous efforts have gone into developing alternative, more effective means of control of Rhizoctonia diseases. Such methods include mulching of fields with certain plant materials or with photodegradable plastic, avoiding application of some herbicides that seem to increase Rhizoctonia diseases in certain crops, and, especially, using biological controls. Rhizoctonia is parasitized by several microorganisms, such as fungi, soil myxobacteria, and mycophagous nematodes. Rhizoctonia also often suffers from the so called Rhizoctonia decline, which is caused by two or three infectious double-stranded RNAs. These RNAs, through anastomoses, spread from infected hypovirulent Rhizoctonia individuals to healthy virulent ones and reduce both their ability to cause disease and their ability to survive. Addition of these agents to Rhizoctonia-infested soil or to seeds, tubers, and transplants before planting in Rhizoctonia-infested soil reduces disease incidence and severity greatly in almost all crops. So far, however, biological controls are still at the experimental stage and are not available for use by farmers. Klasifikasi Rhizoctonia solani sebagai berikut: Kingdom : Fungi Phylum : Basidiomycota Class : Agaricomycetes Order : Cantharellales Family : Ceratobasidiaceae Genus : Rhizoctonia Species : R. Solani Hawar pelepah padi menjadi penyakit yang semakin penting di beberapa negara penghasil padi.Di indonesia, hawar pelepah mudah ditemukan pada ekosistem padi dataran tinggi sampai dataran rendah.Gejala penyakit dimulai pada bagian pelepah dekat permukaan air.Gejala berupa bercak-bercak besar berbentuk jorong, tepi tidak teratur berwarna coklat dan bagian tengah berwarna putih pucat.Semenjak dikembangkan varietas padi yang beranakan banyak dan didukung oleh pemberian pupuk yang berlebihan terutama nitrogen, serta cara tanam

debgan jarak yang rapat menyebabkan perkembangan hawar pelepah semakin parah.Kehilangan hasil padi akibat penyakit hawar pelepah dapat mencapai 30%. Dilihat dari segi biologi dan ekologinya,Penyakit hawar pelepah mulai terlihat berkembang di sawah pada saat tanaman padi stadia anakan maksimum dan terus berkembang sampai menjelang panen, namun kadang tanaman padi di pembibitan dapat terinfeksi parah. Rhizoctonia solani Kuhn termasuk cendawan tanah, sehingga disamping dapat bersifat sebagai parasit juga dapat sebagai saprofit. Pada saat tidak ada tanaman padi, cendawan ini dapat menginfeksi beberapa gulma di pematang juga tanaman palawija yang biasanya digunakan untuk pergiliran tanaman seperti jagung dan kacang-kacangan. Cendawan ini bertahan di tanah dalam bentuk sklerosia maupun miselium yang dorman. Sklerosia banyak terbentuk pada tumpukan jerami sisa panen maupun pada seresah tanaman yang lain. Selama pengolahan tanah sklerosia tersebut dapat tersebar ke seluruh petakan sawah dan menjadi inokulum awal penyakit hawar pelepah pada musim tanam berikutnya.Fenomena ini menunjukkan bahwa sumber inokulum penyakit hawar pelepah selalu tersedia sepanjang musim. Rhizoctonia solani terutama menyerang benih tanaman dibawah permukaan tanah, tetapi juga dapat menginfeksi polong,akar,daun dan batang.Gejala yang paling umum dari Rhizoctonia adalah redaman off, atau kegagalan benih yang terinfeksi untuk berkecambah.Rhizoctonia soloni dapat menyerang benih sebelum berkecambah atau dapat membunuh bibit sangat muda segera setelah terjadi perkecambah.Ada berbagai kondisi lingkungan yang menempatkan tanaman pada risiko tinggi infeksi karena Rhizoctonia patogen lebih suka iklim basah hangat untuk infeksi dan pertumbuhan. Bibit adalah yang paling rentan terhadap penyakit hawar pada pelepah. Siklus penyakit Rhizoctonia solani dapat bertahan dalam tanah selama bertahun-tahun dalam bentuk sclerotio.Sclerotia dari Rhizoctonia memiliki lapisan luar tebal memungkinkan untuk bertahan hidup dan berfungsi sebagai pelindung dari suhu dingin,pathogen juga dapat mengambil bentuk miselium yang berada di permukaan tanah.Jamur tertarik oleh rangsangan kimia yang dilepaskan oleh tanaman yang tumbuh atau residu tanaman membusuk.Proses penetrasi dari sebuah host dapat dicapai dalam beberapa cara.Pathogen dapat melepaskan enzim yang dapat memecahkan dinding sel tanaman,dan terus menjajah dan tumbuh di dalam jaringan yang mati.Ini adalah rincian dari sel dinding dan kolonisasi pathogen dalam host adalah apa bentuk sclerotia tersebut.Baru innoculum diproduksi didalam jaringan host,dan siklusyang baru diulang saat tanaman baru menjadi tersedia.Siklus penyakit dimulai seperti 1) yang sclerotia atau miselium melewati musim dingin pada tanaman puing,tanah atau host. 2) Para hifa muda dan basidia berbuah (jarang) muncul dan menghasilkan miselium dan basidiospora. 3) Produksi sangat jarang dari basidiospora berkecambah menembus stoma sedangkan tanah miselium pada permukaan tanaman dan mengeluarkan enzim yang diperlukan ke permukaan tanaman dalam rangka untuk memulai infeksi dari tanaman inang. 4) Setelah mereka berhasil menyerang miselium host-nekrosik dan membentuk sclerotia dalam dan di sekitar jaringan yang terinfeksi yang kemudian mengarah ke berbagai gejala yang berhubungan dengan penyakit seperti tanah busuk,busuk batang,rendaman dan lain sebagainya. Dilihat dari cara hidupnya patogen dikenal lebih menyukai cuaca yang basah,hangat dan wabah biasanya terjadi pada bulan-bulan awal musim panas kebanyakan gejala patogen tidak terjadi sampai akhir musim panasdan dengan demikian sebagian besar petani tidak menyadari tanaman terjangkit sampai panen.Kombinasi faktor lingkungan telah dikaitkan dengan prevalensi patogen seperti:adanya tanaman inang,curah hujan sering atau irigasi dan suhu meningkat di musim semi dan musim panas.Selain itu, pengurangan drainase tanah karena berbagai teknik seperti pemadatan tanah juga dikenal untuk menciptakan lingkungan yang menguntungkan bagi patogen.Patogen tersebar sebagai sclerotia,dan sclerotia ini dapat berpergian dengan sarana angin,air atau tanah gerakan antara tanaman inang. Pengendalian hawar pelepah padi (Rhizoctonia solani Kuhn) dapat dikendalikan secara kimia,biologi dan teknik budidayanya. Pengendalian secara kimia dengan menggunakan fungisida berbahan aktif benomyl,difenoconazal,mankozeb,dan validamycin dengan dosis 2cc atau 2g per satu liter air dapat menekan perkembangan cendawa R. Solani kuhn Pengendalian secara biologi dengan penyemprotan beberapa bakteri antagonis dapat mengurangi tingkat keparahan hawar pelepah. Penambahan bahan organik yang sudah terdekomposisi sempurna/sudah matang (kompos jerami dengan C/N rasio 10) dengan dosis 2 ton/ha, dapat menekan perkecambahan sklerosia di dalam tanah dan menghambat laju perkembangan penyakit hawar pelepah di pertanaman. Pengendalian dengan teknik budidaya diantaranya yaitu menerapkan jarak tanam tidak terlalu rapat, pemupukan komplit dengan pemberian nitrogen sesuai kebutuhan, serta didukung oleh cara pengairan yang berselang. Cara ini dapat menekan laju infeksi cendawan R. solani pada tanaman padi. Disamping itu, pengurangan sumber inokulum di lapangan dapat dilakukan dengan sanitasi terhadap gulma-gulma disekitar sawah.Pengendalian penyakit hawar pelepah mempunyai peluang keberhasilan yang lebih tinggi bila taktik-taktik pengendalian tersebut di atas dipadukan (pengendalian penyakit secara terpadu). http://antonmhb.lecture.ub.ac.id/2012/06/mengenal-berbagai-penyakit-pada-padi/ th Agrios, George N. 2005. Plant Pathology 5 edition. Burlington. Elsevier Academic Press.