1. introduction...next significant introduction of eucalypts was in the nilgiri hills, tamil nadu,...

280

1. IntroductionEucalypts are one of the major forest plantation species grown internationally andare of prime importance in the southern hemisphere, much of South-East Asia,southern China and the Indian subcontinent. There are more than 700 species ofEucalyptus, mostly native to Australia and very small numbers are found in adjacentareas in New Guinea and Indonesia. Eucalypts have evolved under selection pressurefrom the harsh native environmental constraints and also from their major nativepathogens and pests. Their capacity for faster growth, even on poor sites, growthhabit, yield, ease of vegetative propagation and desirable product qualities have ledto widespread establishment of eucalypt plantations in many countries outside theirnatural range of distribution, including India.

Eucalypt has a long history in India. It was first introduced around 1790 by TipuSultan, the ruler of Mysore, in his palace garden on Nandi Hills in Karnataka. Thenext significant introduction of eucalypts was in the Nilgiri Hills, Tamil Nadu, in1843, and later regular plantations of E. globulus were raised in 1856 to meet thedemands for firewood (Wilson, 1973). Since then, there were several other attemptsto introduce eucalypts in various parts of the country. Most of the eucalyptplantations in India were raised during two decades between 1960-1980. The policyof converting low value natural forests into plantations aimed at improving productivityand to generate government revenue led to raising of fast growing species includingeucalypts during the 1960s, by clear felling natural forests. A much more dynamicprogramme of converting the natural forest into plantations of fast growing specieswas advocated during 1976 and more area were planted with eucalypts. So far, morethan 1 Mha of eucalypt plantations have been established in different states, viz.,Andhra Pradesh, Bihar, Goa, Daman and Deu, Gujarat, Haryana, Karnataka, Kerala,Madhya Pradesh, Maharashtra, Punjab, Tamil Nadu, Uttar Pradesh and West Bengal.Among various species, varieties and provenances of eucalypts tried in India (Bhatia,1984), Eucalyptus hybrid, a natural hybrid of E. tereticornis x E. camaldulensis known

Diseases in Eucalypts:Status and ManagementC. Mohanan

13

281

as ‘Mysore gum’ is the most outstanding and favoured one. Other species ofEucalyptus grown on a large-scale are E. grandis, E. citriodora, E. globulus, and E. camaldulensis. Eucalypt plantations were also raised under various state and centrallysponsored schemes to meet the demands of local people in respect of the requirementsof firewood, small timber, poles, etc. Eucalypts were also accepted as a good farmforestry tree for planting on field bunds, canal sides and in marginal agricultural lands.

Even though, eucalypts in their native environments are hosts to a wide range offungal pathogens, the broad genetic base of individual species and their presence inheterogeneous forest communities, however, provide significant protection againstdisease epidemics. However, large-scale monoculture plantations with narrow geneticbase raised outside their natural distribution range become prone to various diseasehazards. Avoidance of major epidemics of eucalypt diseases requires an increasedawareness of the risks from pathogens and a systematic approach to disease management.A good knowledge on diseases affecting the crop at their various growth phases, possiblepredisposing factors for the disease development and spread and also available short-term and long-term strategies to contain the diseases is warranted. Based on suchknowledge, clones, provenances and Eucalyptus species can be assessed for theirsusceptibility to major pathogens and strategies can be devised for the production andprotection of eucalypt stand. This chapter on diseases of eucalypts in India is an attemptto provide information on diseases affecting the various eucalypt species in plantationsand nurseries and also provides recommendations for disease management.

2. Diseases in PlantationsIn eucalypt plantations, large number of pathogens were recorded causing foliageand stem diseases, while the root diseases were only few. Most of the seriousdiseases occur within the first three years of outplanting. A few diseases are short-lived such as Lasiodiplodia stem canker, while others continue to affect the trees tillthe end of the rotation affecting the growth considerably and consequently yield(Sharma et al., 1985a, b).

2.1. Stem Canker Diseases2.1.1. Pink diseaseThe pink disease is widespread in eucalypt plantations throughout the country withincidence varying from 5 to 75 per cent depending upon the rainfall and microclimaticconditions of the area as well as the species. E. tereticornis and E. camaldulensisare the severely affected species in the low elevated areas, while E. grandis is theimportant species affected in high ranges.2.1.1.1. SymptomsUsually the pink disease affects the two-year-old plants and above, but infection ofone-year-old plants and coppice crops is not uncommon. The pathogen possibly

Diseases in eucalypts: Status and management

282

infects the main stem or branches through the lenticels. Tissues of the inner bark,including cambium are killed and show prominent browning. The first sign of theinfection is the development of cobweb stage of the fungus during the monsoon.Soon pustules, small pin head size white mycelial bodies, develope over the cobweb.The infected area becomes depressed and develop vertical splitting on the bark. Theperfect stage, characterized by the pink encrustation, develops over the infectedarea. Numerous club-shaped basidia with basidiospores, a source of inocula forfresh infection are produced. Oozing of kino from the canker also occurs in certaincases (Fig. 1). The apical shoot above the canker dies when the stem is completelygirdled. Numerous epicormic shoots develop from the healthy stem just below thecanker. The shoots also get infected and killed following wilting and drying up. Oneof these shoots usually survives and becomes a leader shoot, which does notescape the infection in the following season. Thus, infected trees, which appearbushy due to repeated infections became frail and weak. The yield and productivityof plantation reduce considerably as the trees show negative growth.

Infection of older trees (three to four-year-old) usually results in localized cankersand trees are normally not girdled. However, under conducive microclimaticconditions, multiple stem cankers occur on main stem and partial to complete girdlingof the stem occurs. The toxin produced by P. salmonicolor is possibly non-hostspecific (Sharma et al., 1985a, b). Screening of various provenances of Eucalyptusspecies, viz., E. brassiana, E. camaldulensis, E. deglupta, E. grandis, E. microcorys,E. pellita, E. resinifere, E. saligna, E. tereticornis, E. tessellaris, E. urophylla,among others, indicate that none of them, except E. brassiana, were resistant toP. salmonicolor toxins (Sharma et al., 1984a, b; 1985a, b; 1988). The non-host specifictoxins have apparently a high biochemical specificity yet little specificity betweenplant species. This way the pathogen gains full benefit from production of suchtoxins in the broadening of its potential range of hosts (Ferreira and Alfenas, 1977;Mitchell, 1984).2.1.1.2. EtiologyPhanerochaete salmonicolor (Berk. and Broome) Julich (=Corticium salmonicolorBerk and Br.) is the pathogen causing pink disease. The pathogen produces fourstages, viz., cobweb, pustule, pink encrustation (perfect stage) and necator on infectedeucalypts stem.2.1.1.3. Pink disease managementDisease management by fungicides has been an established practice in pink diseaseaffected rubber plantations in India and South-East Asia (Hilton, 1958). Laboratoryand field screening of various fungicides showed that copper fungicides andtridemorph (Calixin) are equally effective in controlling the disease (Seth et al., 1978;Kumar et al, 1979; Sharma et al., 1984a, b; 1985a, b; Mohanan, 1995a). The possiblelong-term solution for managing the pink disease in eucalypts appears to be through

C. Mohanan

283

species selection and tree improvement. Eucalyptus species and progenies fromtrees, which have escaped from infection in high disease incidence areas need to beselected and clonally propagated. However, various clones developed by differentagencies in different parts of the country are not giving very promising results. Theimprovement through hybridization, though time consuming, may also be attemptedfor long-term disease control.

2.1.2. Crysoporthe stem cankerIn India, the disease was first recorded from two-year-old E. grandis plantationsfrom Wayanad Forest Division, Kerala, during 1980s (Mohanan and Sharma, 1982;Sharma et al., 1985a, b). Later the disease was recorded on three- to six-years-oldplanations of E. grandis, E. citriodora, E. deglupta, E. tereticornis, E. torelliana indifferent parts of the Kerala state (Sharma et al., 1985a, b).2.1.2.1. SymptomsThe first symptom of the disease is development of slightly sunken, elongate areasmeasuring about 15-20 cm on the trunk either at the base or above ground, just afterthe south-west monsoon. Observation showed that the tissue beneath the depressedbark (inner bark) was brown and apparently dead. As canker developed during thedry period (December-April), the bark showed vertical splitting, which increased inlength and width with age. Generally, at this time gummosis (oozing of kino) wasobserved in a few of the cankers. However, gummosis was commonly associatedwith the older cankers. The ruby coloured kino was usually washed down duringthe rainy period and imparted a distinct colour to the affected trees by which theycould be recognized easily. Often multiple stem cankers appear on trunk whichbecame confluent to form long cankerous areas. Usually the cankers developedabove the ground level and occasionally at the base. Mortality of trees occurred inE. grandis, E. citriodora and E. deglupta trees (Fig. 2). Disease was also recordedon coppice shoots from E. grandis stumps. Due to infection, the per cent stumpssprouted decreased with the increasing gummosis due to canker at the basal area.2.1.2.2. EtiologyChrysoporthe cubensis (Bruner) Gryzenh. and M.J. Wingf. (= Cryphonectria cubensis(Bruner) Hodges is the pathogen associated with the stem disease. C. cubensis wasfirst reported from Cuba (Bruner, 1917) where it caused stem canker of variouseucalypts. It was not reported again until 1970 when it was reported as Endothiahavanensis Bruner by Boerboom and Maas from Surinam. Subsequently, Hodgesand Ries (1974) also recorded it under the same name from Brazil. It was only latershowed that what was described as E. havanensis from Brazil and Surinam wasDiaporthe cubensis. Bruner and recently Hodges (1980) transferred it to genusCryphonectria. This stem canker disease is widespread and has also been recordedfrom Cuba, Florida, Hawaii, Puerto Rico, Brazil, Surinam, Western Australia, Hong


284

Kong, Cameroons and Venezuela (Boerboom and Maas, 1970; Hodges and Reis,1974; Ferreira et al., 1977, 1978). The distribution of pathogen is probably determinedby the tropical humid climate needed for the growth and spread of the pathogen.

Recent phylogenetic studies based on multiple gene sequence comparisons(Gryzenhout et al., 2004) have revealed that isolates of C. cubensis group separatelyfrom other Cryphonectria species. Within the C. cubensis clade, isolates formedthree distinct subclades that include isolates mainly from South America, SouthAfrica and South-East Asia, respectively. In this study, they established a newgenus, Chrysoporthe, for this species. Chrysoporthe is characterized by superficial,blackened conidiomata, limited ascostromatic tissue and blackened perithecial necksprotruding from the orange stromatal surface (Fig. 3a & b). Although, specimens ofC. cubensis from South East Asia and South America reside in two distinctphylogenetic sub-clades, they could not be separated or distinguished from thetype specimen, originating from Cuba, based on morphological characteristics. Atpresent, these specimens are collectively transferred to Chrysoporthe as a singlespecies, Chrysoporthe cubensis (Gryzenhout et al., 2004).2.1.2.3. Disease managementThe basal cankers are known to reduce the sprouting of stumps by about 10-20 percent. In Kerala, though the frequency of basal cankers was less, about 35 per cent ofthe stumps affected with the disease (indicated by gummosis) failed to producecoppice shoots. It seems that excessive gummosis kills the tissues of the outer barkas do the cankers and thus, brings about sprouting failure. In such plantations, eventhough the mortality was less, the impact of the disease was greater on the coppicecrop. At present the level of canker disease is low, with a maximum mortality of about3 per cent, the anticipated increase in inoculum over the years in the conduciveclimate of the Kerala state could pose a serious threat to eucalypts, as in Brazil. Thelong term control in a forestry crop is possible only either by field selection or bybreeding for resistance. In Brazil, stable resistance to Crysoporthe stem canker hasalready been obtained by intensive field selection followed by clonal propagation.As a first step in this direction more than 40 eucalypts (various provenancesbelonging to different species) are being screened against C. cubensis in Kerala(Sharma et al., 1984a, b; 1985a, b). Brush on application of copper fungicide (1 percent paste) on bark and cut surface of the stumps or application of tridemorph (0.2%a.i.) can control the infection on stem and coppice growth.

2.1.3. Amphilogia stem cankerThis stem canker disease was first recorded from the four-year-old E. grandisplantations in Wayanad Forest Division, Kerala during 1980s (Mohanan and Sharma,1982). Later, it was recorded from E. gandis, E. tereticornis, E. torelliana, E. degluptaplantations in the state (Sharma et al., 1985a, b; Mohanan and Yesodharan, 2005).

C. Mohanan

285

The disease caused twig, branch and main stem cankers. Death of twigs and brancheswas common but it was seldom observed for a tree, except in E. torelliana, whichappeared to be more susceptible than others species. Microthia havanensis(=Cryphonectria gyrosa) was first described as Endothia havanensis from Cuba(Bruner, 1917) on various eucalypts (E. occidentalis, E. botryoides, E. rostrata,E. mycrophylla and E. robusta). Since then, it has been reported in Japan onE. globulus (Kobayashi and Ito, 1956), in Australia on E. marginata (Davison, 1982;Davision and Tay, 1983).2.1.3.1. SymptomsThe infection usually occurs on lower part of the stem, often near the ground duringthe monsoon (June-July) and by September-October depressed areas, 30-40 cm longon the bark become visible. The tissues beneath the canker turned necrotic and getkilled. During the dry period splitting of the bark appeared on cankered areas. Thepycnidia, orange-red in colour, developed over the bark arranged in vertical linearrows or scattered during the wet period (June-September) (Fig. 4a to c). The pycnidiaproduce long orange yellow tendrils of spores during monsoon. Characteristicascomata with log beaks developed during the following dry period (December-April) on the cankered areas, either separately or interspersed with pycnidia. Deathof E. torelliana trees occurred when the cankers girdled them completely. Nogummosis was noticed on the cankers as in the case of C.cubensis canker. Infectionalso occurs on branches and twigs resulting in twig and branch die-back.2.1.3.2. EtiologyAmphilogia gyrosa (Berk. and Broome) Gryzenh., H.F. Glen, H.F. and M.J. Wingf.(= Cryphonrctria gyrosa (Berk. and Br.), Endothia havanensis (Bruner) Baur. Baar(1978) transferred E. havanensis to C. havanensis keeping along with C. parasitica,C. radicalis, C. nitschkei and C. macrospora in a group typified by C. gyrosa. Lateron Hodges (1980) considered E. havanensis as synonyms with C. gyrosa. Recentphylogenetic studies by Gryzenhout et al. (2006) on isolates of C. havanensis oneucalypts in Mexico and Hawaii (U.S.A.) revealed that the isolates resided in agenus distinct from Cryphonectria sensu stricto, and described as Microthia. Thegenera Cryphonectria and Endothia are closely related and recent DNA sequencecomparisons have shown that isolates from Elaeocarpus spp. in New Zealand,previously identified as Cryphonectria radicalis and Cryphonectria gyrosa,represent a phylogenetic group distinct from those including other species ofCryphonectria and Endothia. A new genus, Amphilogia, is described for thecollections of C. gyrosa from Sri Lanka and New Zealand (Gryzenhout et al., 2005,2006, 2009).2.1.3.3. Disease managementEven though A. gyrosa is capable of killing branches and trees, long-term fieldmonitoring revealed that A. gyrosa is a weak pathogen and often it was associated


286

with C. cubensis. In more than six-year-old trees, A. gyrosa caused mild cankerswithout any apparent damage. Only E. torelliana is highly susceptible to A. gyrosacauses and causes ca. 10 per cent mortality (Sharma et al., 1985a, b). Fungicidesevaluated indicate that there are quite a few fungicides like Benlate (0.1% a.i.),Bavistin (0.1% a.i.), Bayleton (0.1% a.i.), Demosan (0.5% a.i) Dithane-M45 (0.5%a.i.), Saprol (0.1% a.i.), Tecto (0.1% a.i.) effective against A. gyrosa, which may beused in controlling the canker disease, should it spread in epidemic proportion(Sharma et al., 1985a, b). Even though, chemical control of this disease is not a long-term solution, till the time we have promising canker resistant/tolerant eucalypts,chemical control may be adopted to check its further spread.

2.1.4. Cytospora stem cankerThe disease, usually causing branch cankers occurs in young E. tereticornis,E. camaldulensis, E. torelliana and E. grandis plantations and the disease incidenceranges from 2.3 to 7.1 per cent. Severe stem infection was recorded on one-year-oldsecond rotation E. tereticornis coppice crops with a mortality rate of 75 per cent.Cytospora eucalypticola has been earlier recorded causing cankers on E. ficifolia,E. globulus and E. marginata in Australia (Gibson, 1975; Davison and Tay, 1983).C. eucalyptina and C. australis have been recorded on different species of Eucalyptusfrom Australia, Portugal, South Africa, Central and East Africa (Azevedo, 1971). Thedisease appears to be favoured by stress conditions for the host. Cytospora stemcanker disease occurs in Uganda, Malawi, Kenya, Pakistan, Myanmar and WesternAustralia (Graces, 1964).2.1.4.1. SymptomsIn the case of branch and twig cankers, infection occurred on any part of the stem.The tissues of the infected region showed pronounced browning and leaves wiltedand defoliated. Numerous black conidiomata (pycnidia) developed scattered overthe entire infected region. Complete girdling of the phloem and cambium usuallyresulted in death of the affected branches. Infection on the main stem of coppiceshoots was initially observed at the base near the stump and later, it graduallyspreads towards the apex. Girdling due to the canker at the base resulted in wiltingof the leaves and death of shoots. In severe case, the infection even spreads toroots killing the stump. Generally, all the shoots of a stump got infected and died.2.1.4.2. EtiologyCytospora eucalypticola van der Westhuzien causes main stem canker and C.eucalypti Sharma and Mohanan causes twig and branch canker. Cytospora, theanamorph of Valsa Fr., sometimes occurs with their ascomatal state, such as Valsaeucalypti and C. eucalypti, although they occur more frequently alone.2.1.4.3. Disease managementSince the disease is now of minor importance, no control measures are recommended.

C. Mohanan

287

2.1.5. Lasiodiplodia stem (root collar) cankerThe disease affects one- to two-year-old E. tereticornis and E. grandis plantations.Infection occurs during the hot, dry months of November-April in Kerala when theday temperature is high (350-380C) and night temperature low (220-250C). Severefluctuations in soil temperature may have caused some injury to the saplings near thecollar region, through which the infection may have occurred. The disease can pose aserious threat in the establishment of young plantations causing as much as 20 percent mortality (Sharma et al., 1985a, b). E. tereticornis is the species most susceptibleto L. theobromae. L. theobromae is a weak parasite, and usually infects the hostthrough wounds. Termites are known to cause problems in the establishment of youngplantations, especially E. tereticornis, in Kerala. In some instances, root injury causedby termites may have acted as entry points for the pathogen.2.1.5.1. SymptomsAffected plants showed typical symptoms of physiological wilting; i.e., droopingapical shoots with flaccid leaves. Within a day or two, the wilted plants died. In allthe diseased plants the root collar region was typically constricted and compressedwith irregular crevices, where occasionally conidiomata of the pathogen wereobserved. Often, the stem above the canker was abnormally swollen (Fig. 5). Thisswelling was the result of the rupturing of the outer bark at the canker resulted ingirdling of the stem and plants died. The tissue in the canker region was brown anddead or dying. Often the infection also extended to roots, causing root decay.2.1.5.2. EtiologyLasiodiplodia theobromae (Pat.) Griffon and Maubl. (=Botriodiplodia theobromaePat.2.1.5.3. Disease managementFungicidal screening against L. theobromae indicated that Bavistin (0.5% a.i) andTecto (0.5% a.i) were most effective (Sharma et al., 1985a, b). Although, chemicalcontrol of disease of this nature in forest plantations is not an economically feasiblesolution, a soil drench of 0.5 per cent a.i. of Bavistin to plants with accidentalinjury may be useful in controlling the disease. As the canker disease ismanifested through wounds, weeding and other soil operations need to be carriedout carefully.

2.1.6. Valsa stem cankerLow incidence of canker disease was recorded in one- to four-year-old E. grandisand E. torelliana plantations in Kerala. The disease caused extensive juvenile twigand branch cankers resulting in die-back of more than 30 per cent of the plants.2.1.6.1. SymptomsGenerally, the cankers are common on twigs and branches and occasionally on mainstem (Fig. 6). Usually the infection is initiated at the base of the branch where a canker


288

develops. Over the dead bark, numerous black fructifications are produced. Often morefructifications are produced on the lower surface of a branch, away from the directsunlight. The affected twigs and branches die due to complete girdling of phloem tissue.2.1.6.2. EtiologyValsa eucalypti Cook and Harness and Valsa eucalypticola Sharma, Florence andMohanan are the causal agents. V. eucalypti and V. eucalypticola are the teleomorphsof Cytospora eucalypti and C. eucalypticola, respectively reported for the firsttime from India on Eucalyptus spp. (Sharma et al., 1985a, b).2.1.6.3. Disease managementSince Valsa spp. mostly cause cankers on lower branches, which eventually die as aresult of natural pruning, it does not appear to be of serious concern.

2.1.7. Macrovalsaria stem cankerThe disease occurs in isolated patches in E. tereticornis plantations in low elevatedareas and E. grandis plantations in medium and high ranges in Kerala. All theaffected trees either die or show wilting of leaves.2.1.7.1. SymptomsGenerally the infection occurs at the basal part of the stem, characterized by a largenumber of black fructifications, scattered over the bark (Fig. 7a and b). The affectedstem develop canker and the underneath tissues show browning. When the stem iscompletely girdled, the foliage wilts and the tree slowly die. Epicormic shootsdevelopment does not occur.2.1.7.2. EtiologyMacrovalsaria megalospora (Mont.) Sivan.2.1.7.3. Disease managementSince the disease is recorded in low incidence, it appears to be of a minor importanceand no control measure is required.

2.1.8. Thyronectria stem cankerThe disease was recorded in E. tereticornis, E. camaldulensis and E. torellianaplantations in Kerala (Sharma et al., 1985a, b). Though the disease was reported tokill the trees in some plantations, it appeared to be unimportant as the incidence wasvery low (>1%). Mortality of trees was recorded mostly from E. tereticornis,E. grandis and E. camaldulensis plantations. Occasionally, branch infection wasalso reported in E. torelliana which killed the shoots outright.2.1.8.1. SymptomsInitially, the conidial state of the pathogen developed near the base of the stemwhich soon spread upwards covering a large area (Fig. 8a to c). The affected tissuesof the stem developed browning and when stem completely girdled, it broughtabout wilting and consequently death of tree. The perfect stage of the fungus was

C. Mohanan

289

formed in loose clusters or scattered over the dead stem. No epicormic shootsdeveloped on the affected trees.2.1.8.2. EtiologyThyronectria pseudotricha (Schw.) Seeler2.1.8.3. Disease managementThough T. pseudotricha is considered to be a wound parasite, no injury/woundswere observed in any of the affected trees examined. The pathogen, causing branchas well as main stem cankers, is capable of killing the trees. As the disease occurs inlow intensity no control measure is required.

2.1.9. Hysterium stem cankerThe disease was reported from four-year-old E. camaldulensis plantations in Kerala(Sharma et al., 1985a, b). All the affected trees died due to girdling of stem by thecanker. H. angustatum commonly occurs on Acer, Alnus, Fagus, Fraxinus, etc., intemperate countries.2.1.9.1. SymptomsThe pathogen caused extensive cankers on branches and upper part of the stem(Fig. 9a to c). The affected tissues of the stem showed pronounced browning. Ondead stem numerous characteristic black fructifications developed, aggregated orsingly.2.1.9.2. EtiologyHysterium angustatum Alb. and Schwein2.1.9.3. Disease managementHysterium canker may be considered as a minor disease of eucalypts because ofthe localized occurrence and low incidence hence, control measure is not required.

2.1.10. Nattrassa stem cankerThe disease was reported from two- to three-year-old E. tereticornis plantations indifferent parts of Kerala (Sharma et al., 1985a, b). The incidence of disease was<1 per cent. The causal agent is a weak pathogen and is known to kill the cambialregion of wide range of plants, including eucalypts, often following injury.2.1.10.1. SymptomsGenerally, the infection appeared on the stem near the ground and later spreadupwards covering a large part of the stem. The infected area got differentiated in adepression, which later turned into a canker. Occasionally, the roots also got infectedand complete girdling of the stem resulted in death of plants. The foliage graduallywilted and defoliated. On the canker numerous minute fructifications, pycnidia, ofthe fungus developed arranged in vertical broken lines. The tissue of the affectedarea showed grayish black discoloration in which dark brown, septate, thick-walled,inter and intra-mycelia were found in abundance.


290

2.1.10.2. EtiologyNattrassa toruloidea (Natrrass) Dyko and Sutton2.1.10.3. Disease managementSince the disease in plantations occurs in low incidence, no control measure isrequired.

2.2. Cylindrocladium Root RotThe disease was recorded from young 9- to 18-month-old E. tereticornis and E. grandisplantations in Kerala. The disease occurred during dry period. About 10 per cent ofthe plants were found to be affected with the disease (Sharma et al., 1985a, b).2.2.1. SymptomsThe leaves of the affected plants became flaccid and apical shoot showed drooping.The leaves turned brown and dried up. The root system of such plants was foundto be completely rotted with pronounced brown discolouration. The affected plantsfailed to survive. On dead roots, abundant mycelium and sporulation of the causalfungus could be observed.2.2.2. EtiologyCalonectria floridana Sobers and its anamorph Cylindrocladium floridanum Sobersand Seymore.2.2.3. Disease managementUnlike other species of Cylindrocladium which cause foliar diseases during the wetseason, occurrence of root rot caused by C. floridanum during the dry period isquite interesting. If the roots of the affected plants are not properly examined, thisdisease may be mistaken either for termite damage or Lasiodiplodia stem canker.Considering the low incidence of this disease, it does not appear to be a seriousproblem and no control measure is required.

2.3. Cylindrocarpon Root RotThe disease was recorded from one-to five-year-old E. tereticornis and E. grandisplantations in Kerala. Even though, the disease incidence in E. grandis plantationswas low (<1%), in E. tereticornis plantations, it was more than 20 per cent during thedry period (Sharma et al., 1985a, b).2.3.1. SymptomsIn E. grandis, the initial symptom was wilting and drying up of leaves. The roots of theaffected trees became discoloured and showed rotting. The infection generally spreadup to the collar area and produced a canker. The affected trees died within one to twomonths. In E. tereticornis, the leaves of the affected plants, especially the bottomones, turned reddish purple in colour and dried up. No wilting of foliage was observed.The plants were killed within two to three weeks after the change in colour of thefoliage was noticed. The roots of diseased trees showed browning and rotting.

C. Mohanan

291

2.3.2. EtiologyCylindrocarpon lucidum Booth state of Thelonectria lucida (Hohn) P. Chaverriand C. Salgado2.3.3. Disease managementC. lucidum is considered to be a weak pathogen as usually the entry in the host isthrough injury or wounds. No control measure is suggested. However, in youngE. tereticornis plantation, the disease appeared to be a potentially serious one as itkilled more than 20 per cent plants, indicating the susceptible nature of the species.

2.4. Vascular WiltWilt disease of E. gandis was recorded during the monsoon (August-September)in one- to two-year-old plantations in Kerala (Sharma et al., 1985a, b). The incidenceof the disease ranged between 10 and 25 per cent, while large-scale mortality wasrecorded in E. grandis plantations in high ranges.2.4.1. SymptomsThe affected plants showed characteristic symptoms of wilting. Initially the lowerfoliage became flaccid and dried up. Slowly and gradually, the wilting proceededupwards eventually killing the growing shoot. The wilted plants could be easilylocated in the plantations because of their dried up leaves. The vascular tissues ofroots and stem of the diseased plants showed typical browning, abundant myceliumand spores characteristic of vascular wilt.2.4.2. EtiologyFusarium oxysporum Schlecht. F. oxysporum, which has a worldwide distribution,is a soil-borne facultative parasite on many plants. It is disseminated throughplant material and soil on implements, transplant, surface drainage, water andwind-borne spores. Infection is mainly through vascular wounds.2.4.3. Disease managementVascular wilt disease in eucalypts was recorded only from a few locations and is notwidespread and hence disease management measure is not recommended.

2.5. Cylindrocladium Shoot BlightCylindrocladium shoot blight affecting leaves and stem of eucalypts is widespreadduring and immediately after the monsoon (June-September), irrespective of age ofplants and species. Stem infection, which is more common in young plants (one- totwo-year-old) and coppice shoots, is observed only during the monsoon, whilethose of leaves is prevalent round the year, especially in humid tracts and highelevation areas such as Wayanad Platteau, Munnar, Idukki and Pamba in Keralastate (Sharma et al., 1985a, b; Mohanan, 1995a, b). Shoot infection caused by variousspecies of Cylindrocladium has been reported from eucalypts growing areas inother states (Reddy, 1973; Bakshi, 1975), Brazil (Figueiredo and Cruz, 1963; Alfenas


292

et al.,1979) and elsewhere (Crous et al., 1998; Crous, 2002). Severity of infectiongenerally depended upon the microclimatic conditions, especially rainfall, humidityand also the age of the plants. Medium to severe infection was recorded in youngerplantations (one- to three-year-old) situated in high rainfall areas irrespective ofspecies of Eucalyptus, whereas in older plantations (four- to eight-year-old), theseverity was usually low. Severe infection of leaves, which caused blight, resultedin extensive premature defoliation. E. tereticornis, E. camaldulensis and E. grandisare the severely affected eucalypt species.2.5.1. SymptomsThe infection affects both stem and foliage. The stem infection, observed in coppiceshoots and branches of young trees, appeared somewhere on branches and causedcanker characterized by a dull brown depression on the stem. During high humid periods,Cylindrocladium was seen to produce profuse mycelium and conidial mass. Theportion of the branch above the canker was killed outright when completely girdled.During the rainy season numerous fructifications (teleomorph) developed on the deadstem. Stem infection coupled with severe leaf blight resulted in die-back of shoots(Fig. 10a & b). New epicormic shoots developed as a result of the die-back, also gotinfected in the subsequent monsoon. Leaves of all maturities from young and oldplants, epicormic and coppice shoots were found to be equally susceptible toCylindrocladium infection. The symptom expression mainly the colour, size and spreadof the lesions varied depending on the leaf maturity and micro- and macro-climaticconditions and Eucalyptus species. In E. grandis, the leaf infection appeared in theform of minute grayish-black spots which coalesced to form large necrotic area. Underhigh humid conditions, the initial spots were usually large grayish black patches, whichspread further at time to cover the entire leaf lamina. In mature leaves occasionally theinfection initiated either from leaf tip and spread downwards or from the margin andgradually spread towards the midrib. During the dry period, the lesions became dullpale brown. Extensive leaf infection caused blight which resulted in premature defoliation.

Cylindrocladium shoot blight occurs in major plantation grown eucalypts, viz.,E. camaldulensis, E. grandis, E. tereticornis, E. urophylla, E. torelliana,E. citriodora, E. deglupta, E. globulus, among others.2.5.2. EtiologyA total of five species of Cylindrocladium were found to be associated with shootinfection of eucalypts. Calonectria quinueseptata Figueiredo and Namekata andits anamorph Cylindrocladium quinqueseptatum Boedijn and Reitsma. Calonectriapyrochroa (Desm.) Sacc. and its anamorph Cylindrocladium ilicicola (Hawley)Boedijn and Reitsma. Calonectria indusiata (Seaver) Crous and its anamorphCylindrocladium theae (Petch) Alf. and Sob. Cylindrocladium clavatum Hodgesand May Calonectria morganii Crous, Alfenas and M.J. Wingf. and its anamorphCylindrocladium scoparium Morg.

C. Mohanan

293

2.5.3. Disease managementControl of Cylindrocladium shoot blight in plantations is not economically feasible.However, the incidence and severity of infection can be brought down to low leveleither by modifying the cultural measures or by chemical application. Importance ofselection of healthy planting stocks as well as selection of appropriate planting timeand schedule according to the rainfall pattern in the planting site is stressed.Mortality in one-year-old plantations due to Cylindrocladium infection can beavoided by planting only healthy seedlings of appropriate age after the onset of pre-monsoon showers or during the first week of the arrival of monsoon. A delay in theplanting programme will facilitate Cylindrocladium infection. A prophylacticfungicidal treatment (Carbendazim 0.2% a.i) of the planting stocks before transportingto the planting site is recommended to check the disease havoc immediately after theplanting (Mohanan, 1995b). Long-term strategies to deal with the Cylindrocladiuminfection in eucalypts include broadening the genetic base of Eucalyptus throughintroduction of more provenances and species with desirable characteristics.

2.6. Phaeoseptoria Leaf SpotThe infection was recorded from eucalypt nurseries and plantations throughout Keralaon E. tereticornis, E. grandis, E. camaldulensis, E. deglupta, E. globulus andE. pellitta (Sharma et al., 1985a, b; Mohanan and Sharma, 1986). Though the diseasewas prevalent in dry season (December to May), yet it was observed even during peakmonsoon period (July-August). Severe infection caused extensive prematuredefoliation. The disease has also been reported from other states (Padaganur andHiremat, 1973) and from other eucalypt growing countries (Kobayashi, 1978).2.6.1. SymptomsThe infection first appeared on mature leaves as purple to brownish purpleamphigenous spots which were characteristically angular and marked by veins,especially on E. grandis and E. tereticornis (Fig. 11). The leaf spots graduallyprogressed upwards and late in the season, they were frequently noticed on youngerleaves. By this time generally, all the mature leaves had defoliated prematurely dueto heavy infection. When the spot turned necrotic, minute black fruiting bodies(pycnidia), generally more on the abaxial surface, developed embedded in the leaftissue. Pycnidia produced long grayish-back tendrils which appear as brownish-black wooly mass on both the leaf surfaces. Due to rain or dew, the conidia gotdispersed from the tendrils and formed a black layer over the leaf surface.2.6.2. EtiologyPhaeoseptoria eucalypti (Hansf.) Walker2.6.3. Disease managementAmong the 13 fungicides evaluated against P. eucalypti, Bavistin, Benlate and Tectowere the most effective ones as they inhibited the growth completely even at 0.1 per


294

cent a.i. Field trials revealed that two applications of Bavistin (0.03% a.i) at weeklyintervals were effective in controlling the leaf infection.

2.7. Coniella Leaf BlightThe leaf disease caused extensive premature defoliation of the lower branches inE. camaldulensis, E. grandis, E. pellita, E. tereticornis, and various clones ofE. tereticornis (Sharma et al., 1985a, b; Mohanan et al., 2010) due to severe infection.Field studies in different eucalypt growing areas in Kerala state suggests that thedisease incidence and severity was greatly favoured by high humidity and moisture.Coniella fragariae is widespread in eucalypt plantations in India, Brazil and thePhilippines (Ferreira et al., 1977; Mohanan, 2010).2.7.1. SymptomsUsually the infection occurred along the leaf margins and tips during the rainy season asmore or less circular lesions with regular margins (Fig. 12). In high humid tracts (>90%r.h.), the infection also developed during dry period. Infection caused by C. fragariaemanifested in the form of circular lesions, which spread to the whole leaf and becamenecrotic and often caused foliage blight. Severe leaf blight and, thereby defoliation wasnoticed in E. camaldulensis, E. grandis and E. tereticornis plantations. Numerous paleto dark brown coloured, immersed to semi-immersed pycnidia of the fungus arrangedmore or less in concentric rings develop over the necrotic lesions. As the necrotic lesionsget enlarged, new rings of pycnidia develop. However, in the case of C. australensis,pycnidia developed irregularly over the necrotic lesions. During the wet period, pale olivegreen to pale brown conidial ooze developed which dispersed by rain splashes and theinoculum spreads to the new healthy leaves. Foliage blight due to severe infection iscommon in eucalypt nurseries and young plantations (Mohanan et al., 2005).2.7.2. EtiologyConiella australiensis Petr, C. castaneicola (Ell. and Ev.) B. Sutton, C. fragariae(Oudem) B. Sutton, C. granati (Sacc.) Petr and Syd. , C. minima B. Sutton and Thaung.2.7.3. Disease managementIn nurseries and young plantations, the disease attained a important status causingsevere premature defoliation, die-back of branches and terminal shoots. The recentfield investigation revealed that Coniella species become dominated over theCylindrocladium species, especially in eucalypt nurseries and plantations situatedin high rainfall (4,000-6,000 mm per annum) of the Kerala state (Mohanan andYesodharan, 2005; Mohanan et al., 2010). Fungicidal application (Dithane M 45(0.2% a.i) is suggested for controlling the disease (Mohanan et al., 2005).

2.8. Guignardia Leaf SpotThe disease has been noticed in E. camaldulensis, E. grandis, E. pellita, E. tereticornisplantations in low and high elevated areas in the Kerala state with a low to medium

C. Mohanan

295

disease severity (Sharma et al., 1985a, b). E.camaldulenis, E. citriodora, Eucalyptusclone KFRI 15, E. deglupta, E. grandis, E. pellita, E. regnans, E. tereticornis, E. torellianaand E. urophylla are the species affected. Guignardia leaf spot disease has earlier beenreported on eucalypt species from South Africa and Malaysia (Gibson, 1975).2.8.1. SymptomsInitially the symptoms developed as minute purplish spots on the upper surface ofthe leaves. Later, they got enlarged and became purplish brown necrotic areas, 4-5mm across, angular to irregular, often lined with veins.2.8.2. EtiologyGuignardia citricarpa Kiely2.8.3. Disease managementThe leaf spot disease is of minor importance and hence, control measures are notsuggested.

2.9. Leaf Spot DiseasesLeaf spot disease caused by various pathogens have been recorded on differentspecies of Eucalyptus from various parts of the country (Sharma et al., 1985a, b).Pestalotiopsis disseminata (Thum.) Steyart, P. guepinii (Desm.) Steyart, P. neglecta(Thum.) Steyart, P. mangiferae (P. Henn.) P. Steyart, P. versicolor (Speg.) Steyart,P. macrospora (Cesati) Steyaert on E. tereticornis, E. torelliana, P. maculans (Corda)Nag Raj, P. metasequoiae (Gucsvicz) Nag Raj, P. palustris Nag Raj, P. tecomicolaNag Raj, P. uvicola (Spegazzini) Bisset (Mohanan and Yesodharan, 2005), Readeriellamirabilis H. and P. Syd. on E. tereticornis, Pestalosphaeria elaedis (Booth andRobertson) van der Aa, Alternaria alternata (Fr.) Kiessler, causing leaf spot inE. camaldulensis, E. citriodora, E. globules, E. grandis, E. pellita, E. tereticornishave been recorded in Kerala (Sharma et al., 1985a, b).

Recently, Alternaria citri Ellis and Pierce apud Pierce causing leaf spot inE. urophylla; Aulographina eucalypti (Cooke and Massee) Aex and E. Mull.causing necrotic leaf spots in E. grandis and E. tereticornis have been recordedfrom Kerala. Chaetomella raphigera Swift on E. camaldulensis, E. tereticornis(Mohanan and Yesodharan, 2005); Colletotrichum acutatum Simmonds,C. dematium (Pers. Ex Fr.) Grov., C. gloeosporioides (Penz.) Sacc., onE. tereticornis; C. crassipues (Speg.) Arz. on E. tereticornis; Cryptosporiopsiseucalypti Sankaran and Sutton, Cryptosporiopsis sp. 1 on E. camaldulensis,E. grandis, E. tereticornis (Mohanan and Yesodharan, 2005), Curvulariaeragrostidis (P. Henn.) J.A. Mayer on E. camaldulensis; Cylindrocladiumcolhounii Peerally on E. camaldulensis; Drechslera state of Cochliobolusspicifer Nelson on E. pellita, Fairmaniella leprosa (Fairm.) Petr. and Syd. onE. grandis and E. tereticornis; Fusarium acuminatum Ellis and Everhart andF. lateritium Nees, F. oxysporum Schlecht, F. moniliforme Sheldon, on E. grandis,


296

E. camaldulensis. Other fungal pathogens causing leaf infection include:Mycosphaerella cryptica Cook and Hansf. on E. tereticornis (Mohanan andYesodharan, 2005), Mycotribula Nag Raj and Kendrick sp. 1, on E. camaldulensis,E. grandis and E. tereticornis (Mohanan and Yesodharan, 2005). Phomopsis eucalypticausing foliage infection on E. grandis, E. tereticornis, E. torelliana (Mohanan andSharma, 1987).2.9.1. Little leaf diseaseLittle leaf disease of eucalypts has been recorded in E. tereticornis, E. grandis andE. globulus plantations throughout Kerala state and elsewhere (Ghosh et al., 1985;Sharma et al., 1985a, b). The disease occurred with low intensity both in nurseriesand plantations. The disease is suspected to be seed-borne. Earlier Sastry et al.(1971) reported a graft transmissible little leaf disease in four- to five-year-oldE. citriodora which was stated to be caused by a virus.2.9.1.1. SymptomsThe affected plants showed prominent stunting and produced much smaller leaveswhen compared to healthy ones (Fig. 13). The new leaves showed considerablereduction in size and became thin, pale, scaly with narrow lamina. The apices of suchleaves often showed browning. The internodes became stunted and all axillary budssprouted resulting in bushy shoots with abnormal minute leaves. Affected trees becameweak due to reduction in stem girth and height growth.2.9.1.2. EtiologyThe disease is caused by phytoplasma (mycoplasma-like organism).2.9.1.3. Disease managementAs the disease is possibly insect transmitted, the plants showing little leaf diseasesymptoms should be uprooted and burnt.

2.9.2. Leaf mosaicA leaf mosaic disease of E. tereticornis was recorded in plantations as well as in nurseries.In nurseries, the disease occurred rarely, however, in plantations invariably a few treeswere always found to be affected with leaf mosaic disease. Incidence of disease wasgenerally very low (<0.1%), except in Thenmala Forest Division where it was 0.5 per cent.2.9.2.1. SymptomsAll the leaves young as well as mature, of the affected plants had mosaic symptoms;i.e., light pale to yellowish white, irregular patches. Even the new leaves showedthese symptoms. The diseased plants did not show any effect on growth, exceptthat affected leaves became leathery and thick.2.9.2.2. EtiologySuspecting that the disease could be viral in nature, standard methods of sap andgraft transmission were attempted on one-year-old seedlings of E. tereticornis butnegative results were obtained.

C. Mohanan

297

2.9.2.3. Disease managementSastry et al. (1971) reported a mosaic disease of E. citriodora caused by tobaccomosaic virus (TMV) from India, which was sap transmissible. The mosaic diseaserecorded from Kerala differs considerably in symptomatology and also in that itcould not be transmitted. Though the disease is not economically important somestudies are warranted to establish the etiology.

2.10. Nursery DiseasesA large number of fungal pathogens are found associated with various diseases ineucalypt nurseries. As most of the nursery diseases are soil-borne, potentialpathogens affect the eucalypt seeds immediately after they begin to germinate.Various diseases namely, damping-off, web-blight, seedling blight, seedling wilt,root-rot and leaf spots appeared almost in succession. Occurrence of web blight,seedling blight and seedling wilt overlapped. Except for the seedling blight, theother diseases continued to affect the seedlings till they were pricked out intopolythene containers. Damping-off, web blight and seedling blight were the majorwidespread diseases in seedbed nurseries. Introduction of root trainers in forestnurseries, where soil-less or soil-free growing medium is used, has had a greaterimpact on incidence of soil-borne diseases in nurseries and also in diseasemanagement.2.10.1. Damping-offBoth pre- and post-emergence damping-off occurred in eucalypt nurseries raisedthroughout the country. Pre-emergence damping-off, though uncommon, often goesundetected because it is misidentified as failure of germination of ‘poor seeds’. Thepost-emergence damping-off occurred more commonly within a week of emergenceof seedlings. The disease spread rapidly with increasing soil moisture, often resultingfrom excessive watering of beds. Mortality of seedlings was observed for the firsttwo-to three-week only.2.10.1.1. SymptomsThe infection caused rotting of the just emerged radicle and subsequently thecotyledons inside the seed coat. The disease occurred within two to three days ofsowing (Fig. 14a). Post-emergence infection caused a collapse of the stem tissuesmarked by a water-soaked constricted area at the soil level causing the seedling tofall over, such seedlings failed to survive. The damping-off usually occurred inroughly circular patches in which the most recently dead seedlings were on theperiphery.2.10.1.2. EtiologyA large number of fungal pathogens are associated with damping-off of eucalyptseedlings. Rhizoctonia solani state of Thanatephorus cucumeris (Frank.) Donk isthe major pathogen. Pythium deliense Meurs., P. myriotilum Drechsler, P. spinosum


298

Saw., Cylindrocladium quinqueseptatum Boedijn and Retsma, C. ilicicola (Hawley)Boedijn and Reisma, C. floridanum Sobers and Seymore, C. parvum Anderson,Fusarium oxysporum Schlecht are the other pathogen associated with damping offin eucalypt seedlings (Sharma et al., 1985a, b).2.10.1.3. Disease managementAs soon as the disease is noticed in seedbeds, watering of beds should be reduced toa bare minimum. Even watering can be avoided for a day or two depending upon theclimatic conditions of the area. Shade over the nursery beds need to be regulated toallow more sunlight over the beds. Fungicides like Bavistin (0.01% a.i), Dithane M 45(0.01% a.i.) should be applied as soil drench at an interval of four hours, in place ofnormal watering. After treatment, watering should be regulated to prevent build up ofexcess soil moisture.

2.10.2. Web blightSeedling web blight of eucalypts, usually occurred in irregular patches in seedbedsand was widespread. Young seedlings are killed outright but older ones remainedalive for some time before dying. The disease, generally appeared within two weeksof seedling emergence.2.10.2.1. SymptomsInitially, the mycelium of the pathogen emerging from the soil grew up on the stem andover the leaves of a few seedlings; and spread to others invading the leaf tissuerapidly (Fig. 14b). The mycelia strands, which were initially hyaline, became lightbrown and branched extensively. Leaves of the infected seedlings developed water-soaked lesions and wilted. Later, they became necrotic and dried up. The stem showedcharacteristic pale grayish-black necrotic lesions. The pathogen often produced off-white to light brown irregular sclerotia on the affected stem and leaves of older seedlings.The fungus also produced its perfect stage on the stem during the rainy season.2.10.2.2. EtiologyRhizoctonia solani Kuhn. state of Thanatephorus cucumeris (Frank.) Donk.2.10.2.3. Disease managementAs soon as the disease is noticed the watering in the seedbeds should be minimized.This will facilitate in checking the spread of the disease. Bavistin or Benlate (0.02%a.i.) can be applied as soil drench for controlling the disease.

2.10.3. Seedling blightSeedling blight usually occurred in one-month-old eucalypt seedlings. The diseaseis widespread in eucalypt nurseries and caused heavy mortality. Seedling mortalityin eucalypt nurseries due to blight disease caused by Cylindrocladium spp. is aserious problem, especially in warm-humid areas of Kerala state (Sharma et al., 1985)and also in other eucalypt growing areas (Bakshi, 1975).

C. Mohanan

299

2.10.3.1. SymptomsInfection on the seedling stem near the soil level, just above the root collar region,was the cause of seedling blight. The affected area became grayish brown killing thetissues and consequently such seedlings dried up. The pathogens produced profuseconidial growth under high humid conditions which helped increasing the inoculumpotential of the pathogens with consequent rapid spread of the disease.2.10.3.2. EtiologyCylindrocladium clavatum, C. colhaunii, C. ilicicola, C. parvum, C. quinqueseptatum,Cylindrocladiella camelliae, C. scoparium are the pathogen associated with the disease.2.10.3.3. Disease managementSeedling blight of eucalypt can be effectively controlled by application of fungicide,Bavistin (0.01% a.i) as foliar and soil drench. If the disease persists due to excessivesoil moisture, another application of the same fungicide may be given.

2.10.4. Coniella seedling blightThe disease occurred in one-to two-month-old E. tereticornis and E. grandisseedlings and caused severe damage to the nursery.2.10.4.1. SymptomsInitially, the symptoms appeared on the leaf tips in the form of browning, which graduallyextended and covered the entire leaf. Numerous black dot-like fructifications of thefungus developed on the necrotic areas. From the leaf, the infection spread to theentire stem, thus killing the seedlings. Later, on the stem also abundant pycnida of thefungus developed. Occasionally, the infection was observed only of stem.2.10.4.2. EtiologyConiella granati (Sacc.) Petrak.2.10.4.3. Disease managementApplication of fungicide, Dithane M45 (0.02% a.i.) as foliar spray can control thedisease in nursery.

2.10.5. Seedling wiltSeedling wilt in eucalypt nurseries was recorded affecting 45- to 60-day-old E. grandisand E. tereticornis seedlings.2.10.5.1. SymptomsThe first sign of the disease was the formation of a white weft of mycelium at the baseof the seedling stem, spreading up to the leaves which may entangle other nearbyseedlings also (Fig. 14c and d). The physiological wilting of seedlings was accompaniedby the development of spherical, off-white sclerotia on the affected leaves and stem.The sclerotia became light brown with age. Wilted seedlings turned brown and died.Usually the infection, which caused decay of the stem and consequent wilting ofplants, was localized on stem and leaves, however, roots remained unaffected.


300

2.10.5.2. EtiologySclerotium rolfsii Sacc. state of Corticium rolfsii Curzi.

2.10.6. Seedling root rotSeedling root rot was recorded from various eucalypt nurseries raised in differentlocations of the Kerala state. The disease affected two-to five-month-old E. grandisand E. tereticornis seedlings.2.10.6.1. SymptomsRoot rot caused slow wilting of seedlings in scattered patches. The first symptomwas the change of pigmentation in apical leaves from normal green to light purple.Within a week, this change in pigmentation moved downwards rapidly and by thetime all the leaves were affected, and apical portion of seedlings showed wiltingsymptoms resulting in death of seedlings. The root system of such plants wasfound to be completely damaged due to rotting. The colour of the affected roots wasdark brown instead of off-white, or pale yellowish brown, the natural colour of roots.Generally, the infection was noticed starting from the feeder roots and later proceedingto the main root system. In some of the root rot specimens even the stem was foundto be affected causing decay of the root collar zone.2.10.6.2. EtiologyCylindrocladium curvatum Boedijn and Reitsma; Sclerotium rolfsii, Rhizoctoniasolani.2.10.6.3. Disease managementThe root rot disease can be effectively managed by drenching fungicide like Bavistin(0.02% a.i) in the seedbeds. The fungicidal application need to be repeated after aweek if the disease persists.

2.10.7. Cylindrocladium leaf spotsLeaf infection, caused by Cylindrocladium spp., is one of the important andwidespread diseases in eucalypt nurseries. Usually, the disease has been recordedto appear after the onset of monsoon. Since under such conditions the pathogenproduces abundant conidia on the affected leaves, which are disseminated bysplashing of rain drops, the disease spreads very rapidly. Nurseries raised at highelevations, the disease appears even before the monsoon. Seedlings of E. grandisand E. tereticornis were highly susceptible to Cylindrocladium spp. (Sharma et al.,1985a, b). This leaf spot disease was also recorded from other parts of the country(Bakshi et al., 1972; Reddy, 1973).2.10.7.1. SymptomsLeaf spots appear first as minute, grayish-black water-soaked lesions on young aswell as older leaves. Later, smaller lesions coalesce to form large necrotic patcheswhich on drying turn brown giving typical blighted appearance. Under high humidity,

C. Mohanan

301

Fig. 3. a: SEM of pycnidium of C. cubensis (385x); b: SEM of ascocarps of C. cubensiscompletely immersed in the bark (120x).

Fig. 1. Pink disease ofEucalyptus.

Fig. 2. Crysoporthe cubensis canker - a general view ofE. grandis plantation showing a dead tree in the centreand thinning of crown of other trees due to disease.


302

Fig. 5. Stem (root collar) cankercaused by L. theobromae.

Fig. 6. A vertical section through ascomata ofV. eucalypticola (60x).

Fig. 4. a. SEM of long spore tendrils from a completely immersed pycnidium ofA. gyrosa (35x), b. pycnidia arranged in vertical rows over the cankered bark andc. vertical section through a pycnidium (70x).

C. Mohanan

303

Fig. 9. Stem canker of eucalypts caused by H. angustatum a. SEM of ascocarp ofHysterium angustatum (45x), b. ascocarp with asci and c. ascospores (400x).

Fig. 7. Stem canker caused by M. megalospora. a. A vertical section through theperithecium showing arrangement of asci and b. ascospores.

a b

Fig. 8. Stem canker of eucalypts caused by T. pseudotricha. a. A magnified view ofconidiomata (880x), b. SEM of conidial head bearing conidia and c. ascocarp with asci.

a b c

a b c


304

Fig. 10. a. Cylindrocladium leaf infection and b. conidia ofCylindrocladium on affected seedling stem.

Fig. 11. Phaeoseptorialeaf infection.

a b

Fig. 13. Little leaf disease.Fig. 12. Coniella leaf infection.

C. Mohanan

305

Fig. 14. Seedling diseases of eucalypts. a. Damped-off patches in seedbeds, b. webblight of E. grandis caused by R. solani and c and d. seedling wilt caused by S. rolfsii.

a b

c d

the initial symptoms are generally large-greyish-black spots, sometimes coveringthe entire leaf; abundant conidia may also be observed on the affected areas. Severeleaf infection causes leaf blight, resulting in premature defoliation, which weakenthe seedlings.2.10.7.2. EtiologyCylindrocladiella camelliae, C. clavatum, C. colhaunii, C. ilicicola,Cylindrocladium quinqueseptatum, (Venkataram and C.S.V. Ram) Boessew.2.10.7.3. Disease managementFungicidal application (Bavistin @ 0.01% a.i.) as foliar drench is found to be highlyeffective in controlling the disease. In case of severe infection, a second treatmentmay be essential after a week interval.


306

2.10.8. Seedling stem infectionSeedling stem infection, often resulting in stem canker occurred in two- to three-month-old E. grandis and E. tereticornis seedlings. The disease was found moreprevalent in E. grandis nurseries raised in high ranges.2.10.8.1. SymptomsInitially the infection developed on the lower half of the stem and later it spread toupper parts as well. The affected seedlings which primarily showed typical symptomsof physiological wilting, such as flaccidity of leaves and the apical shoot, wereeventually killed. Under high humid-warm conditions abundant conidia ofCylindrocladium were observed on the infected stem. Development of epicormicroots and shoots from the callus was frequently observed during continuous rainyperiods.2.10.8.2. EtiologyCylindrocladium clavatum, C. ilicicola, C. quinquespetatum

2.10.9. Rhizoctonia collar rotThe disease occurred in seedbeds with high seedling density under high humidityand air stagnation due to crowding of seedlings. The disease was recorded in two-to three-month-old E. grandis and E. tereticornis seedlings.2.10.9.1. SymptomsThe infection appeared just near the ground level in the form of grayish water-soaked lesions on the seedling stem. This discoloration was soon followed bysplitting of the outer bark, stem girdling and callus formation. The affected seedlings,which showed typical symptoms of physiological wilting, failed to survive.2.10.9.2. EtiologyRhizoctonia solani

2.10.10. Shoot blightThis is a common disease in eucalypt nurseries raised throughout the country. Thedisease affects most of the Eucalyptus species. In Kerala, the disease was moreprevalent in high rainfall areas than in low rainfall areas. Shoot blight has beenrecorded to cause over 50 per cent of mortality of containerized seedlings. Thisdisease also affects the root trainer nurseries (Mohanan et al., 2005).2.10.10.1. SymptomsShoot blight of eucalypt seedlings was caused due to multiple infection byCylindrocladium affecting the apical buds, stem (causing stem canker) and leaves.Generally, more than one species of Cylindrocladium were associated with thedisease. Affected seedlings, which became leafless, were killed outright.2.10.10.2. EtiologyCylindrocladium clavatum, C. ilicicola, C. quinqueseptatum

C. Mohanan

307

2.10.10.3. Disease managementBavistin 0.01 per cent a.i. applied as foliar and soil drench is found to be highlyeffective in controlling the shoot blight disease. In case of severe infection, a secondtreatment may be essential after a week.

2.10.11. Phaeoseptoria leaf spotThis disease was prevalent in E. grandis, E. tereticornis nurseries during the monthsof March-May. Severe infection caused defoliation of mature leaves thus affectingthe growth of seedlings.2.10.11.1. SymptomsThe infection appeared initially on the mature leaves as purple to brownish-purpleamphigenous angular spots. The leaf spots gradually progressed upwards affectingeven the youngest leaves. In dry weather, when the spots turned necrotic, minuteblack pycnidia developed embedded in the leaf tissue. These pycnidia producedabundant conidia, usually in tendrils, which appeared as brownish-black woolymasses on both the leaf surfaces.2.10.11.2. EtiologyPhaeoseptoria eucalypti (Hansf.) Walker

2.10.12. Disease management in nurseriesThe diseases in eucalypt nurseries are caused by several pathogenic fungi and it isnot possible to control them by one fungicide or specific combined application ofdifferent fungicides. Though control measures for some of the important diseasesare given at appropriate places, experience gained during the disease survey andchemical control trials indicate that the nursery disease complex affecting eucalyptseedlings can be controlled effectively by an integrated approach; i.e., propermanagement of the nursery together with some prophylactic application of fungicides.

Proper management of nursery includes adequate shade with dispersed light,medium density of seedlings and the right quantity of water per seedbed (30-40litre a time per standard bed, 12 m x 1.2 m). The frequency of watering shouldrange from two to four times a day depending on the climatic conditions andgrowth stage of seedlings. These measures, if properly followed, will preventthe appearance of diseases to considerable extent and also check thedevelopment of disease into serious epidemic proportions. Prophylacticapplication of effective fungicides at the proper time will control the developmentof these diseases effectively.2.10.12.1. Root trainer nurseries and disease managementDuring the past few years, forest nursery practices in India have undergone atremendous modifications based on various microclimatic, edaphic and biotic factors,including host, pest and pathogen association (Mohanan, 2000a, b). Consequently,


308

seedling health has been given more importance which further widened the scope ofphytosanitary problems. However, introduction of root trainers in forestry sectorand thereby the technological changes in seedling production has had a majorimpact on nursery management (Mohanan, 2003). As soil less or soil-free pottingmedia are used in root trainers, common soil-borne diseases such as damping-off,seedling blight, wilt, etc. seldom occur in root trainer nurseries. Another advantageis in root trainers, the seedlings require a maximum period of 90 days growth andhence rigorous management is possible during this comparatively short period ofmaintenance than in conventional nurseries, where seedlings have to be maintainedfor two to four months. For example, eucalypt seedlings have to be maintained in theseedbeds for three to four months and, thereafter, in polythene containers for two tothree months. In root trainer nurseries, even if foliage disease occurs, the affectedseedlings can be easily removed from the blocks and replaced with other healthyseedlings, thereby avoiding the spread of disease in nursery. Since the root trainerseedlings exhibit uniform growth performance, prophylactic fungicidal treatment, ifrequired, and maintenance of seedling quality are easier than in conventional nurserysystem (Mohanan, 2003). Exploitation of the potential of clonal forestry has resultedin increased productivity of eucalypts in countries like Brazil, South Africa andCongo (Zobel, 1993). In India, clonal forestry on a large-scale was started in AndhraPradesh state by ITC Paper Boards Ltd. during 1980s. Eucalypt plus trees wereselected from the plantations and ramets were prepared on a large-scale for raisingplantations under farm forestry and regular forestry programmes (Piare Lal, 1993). InKerala state also, clonal forestry initiated recently and many disease resistant clonesof eucalypts were identified and ramets were prepared on a large-scale (Balasundaranet al., 2000). Eucalypt seedlings and clonal plants can be conveniently grown in roottrainers. The technology offers production of uniform sized, disease free and healthyplanting stock.

3. Discussion and ConclusionDuring its short rotation period of six to eight years, eucalypt suffers from a largenumber of diseases showing its vulnerability to indigenous pathogens to which ithas never been exposed to in its natural habitat. Diseases in plantations areeconomically important as they affect wood production, both qualitatively andquantitatively. While outplanting of nursery stock to the field may be expected tobe accompanied by a decline in the variety and the impact of diseases, the conversemay also occur as the age-related changes in host morphology and physiologymake it susceptible to fresh parasites. In the plantations, effect of monoculture isfound usually more pronounced in causing serious diseases of stem, especiallycanker diseases, than of foliage. The stem cankers like pink disease, Crysoporthestem canker were the most serious ones as they either killed the affected trees or

C. Mohanan

309

retarded the growth considerably. Outbreak of pink disease in E. grandis is importantas this species was earlier considered to be resistant. At present, Crysoporthe stemcanker is a potentially serious disease of eucalypts in Kerala. The disease wasalready known to be of major significance in Brazil, South Africa, etc. Though themortality of eucalypts in Kerala caused by the disease is very less (ca 3%), itsoccurrence in Kerala has to be taken seriously as it may spread in epidemic proportionas in Brazil after building up of inoculum. Although, E. grandis grown in Keraladoes not appear to be as susceptible as E. saligna in Brazil.

The other significant disease, Cytospora stem canker caused byC. eucalypticola which has caused heavy mortality in South Africa and elsewhere,was recorded in Wayanad killing about 65 per cent of the coppiced shoots ofE. tereticornis. This species has not been found to cause mortality in plains, whereE. tereticornis is the major species. However, considering its potential in killingtrees outright this disease also need surveillance. Lasiodiplodia stem canker, apotentially serious disease in young plantations is mostly related to managementpractices. If cultural practices are improved, occurrence of this disease can be avoidedconsiderably. In eucalypt plantations, Cylindrocladium leaf blight caused byCylindrocladium spp. has emerged as a major problem, especially plantations situatedin high rainfall areas. The problem was more severe in plantations with tapiocaraised as intercrop. Apparently the plants do not suffer much damage from thedefoliation as they give rise to new flush after the monsoon. However, infection ofbranches and main stem, which often killed the plants up to two-year-old and coppiceshoots, was damaging (Mohanan, 1995b). Such severe infection is facilitated byprolonged high humidity due to incessant rains for two to three months. In this way,Cylindrocladium which is a minor pathogen of eucalypts in Australia poses a seriousproblem in nurseries and plantations in Kerala.

High incidence of disease was recorded in nursery due to increased proximitybetween host units and improper nursery management practices which provideconducive microclimatic conditions (Mohanan, 2000a, b). This is evident from thefact that disease incidence declines or disappears altogether after the stock istransplanted to the field. In eucalypt nurseries, Cylindrocladium spp. are the mainserious pathogens as they caused considerable mortality of seedlings. Besides,facultative parasites like R. solani and S. rolfsii have also emerged as the seriouspathogens. It becomes clear that indigenous pathogens with wide host range, whichhave adopted the introduced eucalypts in Kerala, have attained a status of seriouspathogens. Besides the susceptibility of eucalypts to these pathogens in the newenvironment, the warm-humid climatic condition of Kerala has also played animportant role in various kinds of fungi adopting eucalypts (Mohanan, 2003; 2009;Mohanan and Sharma, 2005). Biological control of Cylindrocladium diseases in forestnurseries employing antagonistic fungi like Trichoderma harzianum and T. viride


310

was also attempted (Mohanan, 2007). The recent introduction of root trainertechnology in forestry sector has a major impact on seedling production system aswell as nursery disease management (Chacko et al., 2002; Mohanan, 2000a, b). Mostof the soil-borne diseases can be avoided in root trainers as soil-less or soil-freepotting media are used in root trainer cells. Foliage diseases caused by air-bornepathogens can also be managed effectively in root trainer nurseries.

ReferencesAlfenas, A.C.; Marsuoka, K.; Ferreira, F.A. and Hodges, C.S. 1979. Identificao

caracteristicas culturais e patogenicidade detres species de Cylindrocladiumisoladas de manchas de folha de Eucalyptus spp. Fitopatalogia Brasileira,4: 445-459.

Azevedo, N.F. dos s de.1971. Forest tree diseases. Oeiras, Laboratorio de PatologiaFlorestal Secretaria de estado da Agricultura. pp.10-33.

Baar, M.E. 1978. The Diaporthales in North America with emphasis on Gnomoniaand its segregates. Mycologia Memoir, 7: 232.

Bakshi, B.K. 1975. Forest pathology: Principles and practices in forestry. Delhi,Controller of Publications. 400p.

Bakshi, B.K.; Reddy, M.A.R.; Puri, Y.N. and Singh, Sujan. 1972. Forest disease survey.Final technical report. Dehradun, FRI. 117p.

Balasundaran, M.; Maria Florence, E.J. and Sharma, J.K. 2000. Raising planting stockof Eucalyptus clones for the Kerala Forest Department. KFRI ResearchReport No. 180. Peechi, KFRI.

Bhatia, C.L. 1984. Eucalyptus in India - Its status and research needs. IndianForester, 110(2): 91-96.

Boerboom, J.H.A. and Mass, P.W.T. 1970. Cankers of Eucalyptus grandis andE. saligna in Surinam caused by Endothia havanensis. Turrialba, 20: 94-99.

Bruner, S.C. 1917. Una Enfermidad gangrenosa de les Eucaliptos. Boleteni No. 37.Santiago de las Vegas, Estacion Experimental Agronomica. 38p.

Chacko, K.C.; Pandalai, R.C.; Balasundaran, M.; Mohanan, C.; Varma, R.V.;Kallarackal, Jose; Sujatha, M.P. and Kumaraswamy, S. 2002. Standardizationof root trainer technology for Tectona grandis, Eucalyptus teretcornis,E. grandis, E. globules, E. camadulensis, Acacia auriculiformis,A. mangium and Paraserianthes falcataria, etc. KFRI Research ReportNo. 229. Peechi, KFRI. 294p.

Crous, P.W. 2002. Taxonomy and pathology of Cylindrocladium (Calonecria) andallied genera. Minnesota, APS Press.

Crous, P.W.; Wingfield, M.J.; Mohammed, C. and Yuan, Z.Q. 1998. New foliarpathogens of Eucalyptus from Australia and Indonesia. MycologicalResearch, 102(5): 527-532.

C. Mohanan

311

Davison, E.M. 1982. Endothia havanensis on jarrah. Australasian Plant Pathology,11(1): 10-11.

Davison, E.M. and Tay, F.C.S. 1983. Twig, branch and upper trunk cankers ofEucalyptus marginata. Plant Disease, 67(11): 1285-1287.

Ferreira, F.A. and Alfenas, A.C. 1977. Pink disease in Eucalyptus spp. caused by Corticiumsalmonicolor Berk. and Br. in Brazil. Fitopatalogia Brasileira, 2(2): 109-115.

Ferreira, F.A.; Alfenas, A.C. and de Freita, A.L. 1978. Determinaco da Resistencia de16 procedencias de Eucalyptus ao cancro causado por Diaporthe cubensisBruner, no Vale do Rio Docc. ReVista Arvore, 2: 119-129.

Ferreira, F.A; Reis, M.S.; Alfenas, A.C. and Hodges, C.S. 1977. Avaliacada Resistenciade Eucalyptus spp. ao cancro causado por Diaporthe cubensis Bruner.Fitopatologia Brasileira, 2: 225-241.

Figueiredo, M.B. and Cruz, B.P.M. 1963 Occurrence of Cylindrocladium ilicicolaon Eucalyptus spp. in the state of Sao Paulo. Arguivos do InstitutoBiologico, 30: 29-32.

Gibson, I.A.S. 1975. Diseases of forest trees widely planted as exotics in the tropics andsouthern Hemisphere. Part 1: Important members of Myrtaceae, Leguminosae,Verbanaceae and Meliaceae. Oxford, Commonwealth Mycological Institute. 51p.

Gosh, S.K.; Mohammed Ali, M.I. and Balasundaran, M. 1985. Light and fluorescentmicroscopic studies on little leaf disease of Eucalyptus. Journal ofPhytopathology, 110(3): 207-212.

Garces, O. 1964. Las enfermedades de los arboles forestales en la America Latina ysu impacto en la produccion forestall. In: FAO/IUFRO Symposium onInternationally Dangerous Forest Disease and Insects, Oxford, 20-30 July1964. Proceedings. The author.

Gryzenhout, M.; Myburg, H.; Hodges, C.S.; Wingfield, B.D. and Wingfield, M.J.2006. Microthia, Holocryphia and Ursicollum, three new genera onEucalyptus and Coccoloba for fungi previously known as Cryphonectria.Studies in Mycology, 55(1): 35-52.

Gryzenhout, M.; Glen, H.F.; Wingfield, B.D. and Wingfield, M.J. 2005. Amphilogiagen.nov. for Cryphonectria like fungi from Elaeocarpus spp. in NewZealand and Sri Lanka. Taxon, 54(4): 1009-1021.

Gryzenhout, M.; Myburg,H.; van der Merwe, N.A.; Wingfield, B.D. and Wingfield,M.J. 2004. Chrysoporthe, a new genus to accommodate Cryphonectriacubensis. Studies in Mycology, 50: 119-124.

Gryzenhout, M.; Wingfield, B.D. and Wingfield, M.J. 2009. Taxonomy, phylogenyand ecology of bark-inhabiting and tree-pathogenic fungi in theCryphonectriaceae. St. Paul, MN, APS Press. 136p.

Hilton, R.N. 1958. The pink disease of Hevea caused by Corticium salmonicolor Ber.and Br. Journal of the Rubber Research Institute of Malayasia, 15: 275-292.


312

Hodges, C.S. 1980. The taxonomy of Diaporthe cubensis. Mycologia, 72: 542-548.Hodges, C.S. and Reis, M.S. 1974. Identificaco do fungo causado de cancro de

Eucalyptus spp. no Brasil. Brasil Florestal, 5(19): 14.Kobayashi, T. 1978. Notes on the Philippine fungi parasitic to woody plants.

Transactions of the Mycological Society of Japan, 19(4): 373-381.Kobayashi, T. and Ito, K. 1956. Notes on the genus Endothia in Japan. I. Species of

Endothia collected in Japan. Bulletin of the Government Forest ExperimentStation, Meguro, 92: 87-97.

Kumar, D.; Nair, J.M.; Thankamma, L.; Deo, A.D. and Mohanan, C. 1979. Annualreport on status of diseases and their control. Kerala, EFI Unit. 128p.

Piare Lal. 1993. Economics of mass clonal multiplication of forest trees. In: RegionalSymposium on Recent Advances in Mass Clonal Multiplication of ForestTrees for Plantation Programmes, Bogor, 1-8 December 1992. Proceedingsedited by J. Davidson. Rome, FAO. pp. 327-343.

Mitchell, R.E. 1984. The relevance of non-host specific toxin in the expression ofvirulence by pathogens. Annual Review of Phytopathology, 22: 212-245.

Mohanan, C. 2000a. Introduction of rootrainer technology in forestry - Impact ofnursery disease management. In: 4th Meeting of IUFRO Working PartyS7.03.04, Finland, 25-28 July 1999. Diseases and insects in forest nurseries.Abstracts edited by A. Lilja and J. Sutherland. pp. 49-50.

Mohanan, C. 1995a. Investigations on outbreak of pink disease in HNL 1994Eucalyptus grandis plantations in Munnar, Kerala, India. ConsultancyReport No. 1. Peechi, Kerala Forest Research Institute. 19p.

Mohanan, C. 1995b. Large-scale mortality of Eucalyptus grandis in 1994 and 1995HNL plantations in grasslands at Pamba. Consultancy Report No.2. Peechi,Kerala Forest Research Institute. 14p.

Mohanan, C. 2000b. Status of forest nursery diseases in India and emerging trendsin seedling disease management. In: 4th Meeting of IUFRO Working PartyS7.03.04, Finland, 25-28 July 1999. Diseases and insects in forest nurseries.Abstracts edited by A. Lilja and J. Sutherland. pp. 31-42.

Mohanan, C. 2003. Modernization of forest tree seedling production system in Indiaand its impact on seedling health, stand establishment and productivity.In: Conference on Nursery Production and Stand Establishment of BroadLeaves to Promote Sustainable Forest Management, 7-10 May 2001.Proceedings edited by L. Ciccarese; S. Lucci and A. Mattson. Italy, APAT.pp. 89-96.

Mohanan, C. 2007. Biological control of seedling diseases in forest nurseries inKerala. Journal of Biological Control, 21(2): 189-195.

Mohanan, C. 2009. Forest health management in India: Present scenario and futurechallenges. In: Asia and the Pacific Forest Health Workshop Forest Health

C. Mohanan

313

in a Changing World, Malaysia, 1-3 December 2008. Abstracts. IUFRO WorldSeries. Vol. 24. Austria, IUFRO. pp. 45-48.

Mohanan, C. and Sharma, J.K. 1982. A serious disease of Anacardium occidentaleL. caused by Cylindrocladium camelliae and its possible control. In: 5th

Symposium on Plantation Crops, Kasaragod, 15-18 December 1982.Proceedings. Kasaragod, CPCRI. pp. 527-532.

Mohanan, C. and Sharma, J.K. 1984. Calonectria theae Loos and its anamorphCylindrocladium theae (Petch) Alf. and Sob. a new record on Eucalyptusfrom India. Current Science, 53(15): 824-825.

Mohanan, C. and Sharma, J.K. 1985. Cylindrocladium causing seedling diseases ofEucalyptus in Kerala, India. Transactions of the British MycologicalSociety, 84(3): 538-539.

Mohanan, C. and Sharma, J.K. 1986. Bipolaris spicifera and Exserohilum rostratumcausing leaf spots of Eucalyptus tereticornis - New record from India.Current Science, 55(19): 990-992.

Mohanan, C. and Sharma, J.K. 1987. Phomopsis eucalypti and Bartalinia terricola,a new pathogen records on eucalypts from India. Transactions of the BritishMycological Society, 88(1): 125-126.

Mohanan, C. and Sharma, J.K. 2005. Improvement of seedling production system inthe forestry sector India and its impact on seedling health and standestablishment. In: 5th Meeting of IUFRO Working Party S7.03.04, Peechi, 6-8 May 2003. Diseases and insects in forest nurseries: Proceedings editedby A. Lilja; J.R. Sutherland; M. Poteri and C. Mohanan. Helsinki, FinnishForest Research Institute. pp. 77-82.

Mohanan, C. and Yesodharan, K. 2005. Biodiversity of plant pathogenic fungi in theKerala part of the Western Ghats. Final report of the project No. KFRI 375/01. Peechi, Kerala Forest Research Institute. 333p.

Mohanan, C.; Rajesh Kumar, K.C. and Yesodharan, K. 2010. Coniella causing foliagediseases in forest species in Kerala, India. Indian Journal of Forestry, 33(3):355-360.

Mohanan, C.; Ratheesh, N.; Laya P. Nair, Rajesh Kumar, K.C. 2005. Disease problemsin root trainer forest nurseries in Kerala State and their management. In: 5th

Meeting of IUFRO Working Party S7.03.04, Peechi, 6-8 May 2003. Diseasesand insects in forest nurseries: Proceedings edited by A. Lilja; J.R.Sutherland; M. Poteri and C. Mohanan. Helsinki, Finnish Forest ResearchInstitute. pp. 7-12.

Padaganur, G.M. and Hiremath, P.C. 1973. Phaeoseptoria eucalypti Hansf. A newrecord to India. Mysore Journal of Agricultural Sciences, 7(2): 336-338.

Reddy, S.M. 1974. Perithecial stage of Cylindrocladium ilicicolla Boed. and Reit.Current Science, 43(2): 57-58.


314

Sastry, K.S.M.; Thakur, R.N.; Gupta, J.H. and Pandotra, V.R. 1971. Three virus diseasesof Eucalyptus citriodora. Indian Phytopathology, 24; 123-126.

Seth, S.K.; Bakshi, B.K.; Reddy, M.A.R. and Singh, Sujan. 1978. Pink disease ofEucalyptus in India. European Journal of Forest Pathology, 8(4): 200-216.

Sharma, J.K.; Florence, E.J.M.; Sankaran, K.V. and Mohanan, C. 1988. Differentialphytotoxic response of cutshoots of eucalypts to culture filtrates of pinkdisease fungus, Corticium salmonicolor. Forest Ecology and Management,24(2): 97-111.

Sharma, J.K.; Mohanan, C. and Maria Florence, E.J. 1985a. Occurrence ofCryphonectria canker disease of Eucalyptus in Kerala, India. Annals ofApplied Biology, 106(2): 265-276.

Sharma, J.K.; Mohanan, C. and Florence, E.J.M. 1985b. Disease survey in nurseriesand plantations of forest tree species grown in Kerala. KFRI research reportNo. 36. Peechi, KFRI. 268p.

Sharma, J.K.; Mohanan,C. and Maria Florence, E.J. 1984a. Nursery diseases ofEucalyptus in Kerala. European Journal of Forest Pathology, 14(2): 77-89.

Sharma, J.K.; Mohanan, C. and Maria Florence, E.J. 1984b. Outbreak of pink diseasecaused by Corticium salmonicolor in Eucalyptus grandis in Kerala, India.Tropical Pest Management, 30(3): 253-255.

Wilson, J. 1973. The need for a rational utilisation of the montane temperate forestsof South India. Indian Forester, 99(12): 707-716.

Zobel, B.J. 1993. Clonal forestry in eucalypts. In: Ahuja, M.R. and Libby, N.J. Eds.Clonal forestry. Vol. 2: Conservation and application. Berlin, Springer Verlag.pp. 134-144.

C. Mohanan

1. introduction...next significant introduction of eucalypts was in the nilgiri hills, tamil nadu,...

Documents