Disease Competitor Moulds Dr. S.R. Sharma

Diseases and Competitor Moulds ofMushrooms and their Management

Technical Bulletin

S.R. SharmaSatish Kumar

V.P. Sharma

National Research Centre for Mushroom(Indian Council of Agricultural Research)

Chambaghat, Solan-173 213 (HP)

Printed : 2007, 1000 Copies

Published by :DirectorNational Research Centre for Mushroom (ICAR)Chambaghat, Solan 173 213 (HP), INDIAPhone: 01792-230451; Fax: 01792-231207E-mail: [email protected]; [email protected]: nrcmushroom.org

N.R.C.M. 2007All rights reserved. No part of this technical bulletin may be reproduced inany form or by any means without prior permission in writing from thecompetent authority.

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CONTENTS

Page No.

Foreword v

1. Introduction 1

2. Fungal Diseases and Competitor Moulds 2

A. Button Mushroom 2

B. Oyster Mushroom 36

C. Paddy Straw Mushroom 38

D. Other Mushrooms 39

3. Viral Diseases 44

4. Abiotic Disorders 65

5. Bacterial Diseases 70

6. References 77

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FOREWORD

The cultivation of Mushrooms is a carefully controlled biological system,however contamination with microorganisms, which are in ways, isinevitable. In India majority of the mushroom holdings are lacking adequatecompost preparation, pasteurization and proper environmental controlfacilities, which lead to the development of various diseases and pestssufficiently to a level to cause considerable yield loss. It is therefore veryimportant for the mushroom growers that they should know the importanceof diseases and competitors and should understand the importance ofhygiene to grow mushrooms successfully and profitably. I would like toadvise the mushroom growers to pay maximum attention to preparecompost/ substrate of optimum quality and maintain highest level of hygieneto avoid these problems. I appreciate the efforts and labour put in by theauthors in compiling and editing the bulletin for its use by the mushroomgrowers and researchers.

Rajendra Prasad TewariDirectorNational Research Centre forMushroom, Solan 173 213 (HP)

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I. INTRODUCTION

Like all other crops, mushroomsare also affected adversely by a largenumber of biotic and abiotic agents/factors. Among the biotic agents,fungi, bacteria, viruses, nematodes,insects and mites cause damage tomushrooms directly or indirectly. Anumber of harmful fungi areencountered in compost and casingsoil during the cultivation of whitebutton mushroom. Many of theseact as competitor moulds therebyadversely affecting spawn runwhereas others attack the fruitbodies at various stages of cropgrowth producing distinct diseasesymptoms. At times there iscomplete crop failure dependingupon the stage of infection, qualityof compost and environmentalconditions. General distribution ofvarious competitor moulds andpathogenic fungi is as follows:

I. Those occurring mainly incompost include: Olive greenmould (Chaetomium olivaceumand other spp.), Ink caps(Coprinus spp.) Green moulds(Aspergillus spp. Penicillium spp.and Trichoderma spp.), Blackmoulds (Mucor spp., Rhizopus

spp.) and other (Myriococcumpraecox, Sporotrichum sp.,Sepedonium sp., Fusarium spp.,Cephalosporium spp., Gliocaldiumspp., and Papulospora spp.).

II. Fungi occurring in compost and incasing soil: White plaster mould(Scopulariopsis fimicola): Brownplaster mould (Papulosporabyssina), Lipstick mould(Sporendonema purpurescens),False truffle (Diehliomycesmicrosporus) and green moulds.

III.Fungi occurring on and in casing soiland/or on the growing mushrooms:Cinnamon mould (Pezizaostracoderma), wet bubble(Mycogone perniciosa), Dry bubble(Verticillium fungicola), Cobweb(Cladobotryum dendroides), Pinkmould (Trichothecium roseum) andgreen moulds.

IV. Fungi attacking the fruit bodies only:Fusarial rot (Fusarium spp.).

At any phase of growth anundesirable growth or developmentof certain moulds can occur and canadversely affect the final mushroomyield.

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II. FUNGAL DISEASES AND COMPETITORMOULDS

A. WHITE BUTTON MUSHROOM(Agaricus bisporus, A.bitorquis)

a. Diseases

1. DRY BUBBLE

Pathogen : Verticillium fungicola

Common Name : Verticilliumdisease, brown spot, fungus spot, drybubble, La mole.

This is the most common andserious fungal disease of mushroomcrop. If it is left uncontrolled, diseasecan totally destroy a crop in 2-3 weeks(Fletcher et al. 1986). Verticilliumfungicola was major pathogenresponsible for considerable yieldlosses of cultivated mushrooms inManchuela area provinces of Cuencaand Albacete, Spain (Gela, 1993). Ina disease survey of commercialmushroom houses, V.malthousei wasisolated from 11.3% of mushroomsampled (Foree et al. 1974). FromIndia the first report of the heavyincidence of dry bubble disease wasfrom mushroom farms located atChail and Taradevi (Seth et al. 1973).

The pathogen has been invariablyisolated from the compost and casingsamples collected from mushroomfarms in Haryana, HP and Punjab(Sharma, 1992). Thapa and Jandaik(1984-85) have recorded theincidence of dry bubble from 25-50%at Solan and Kasauli and upto 15%at Shimla and Chail during 1980-81.Artificial inoculation with thepathogen at the time of spawningand at different loads of inoculumhad delayed pinhead formation by 5days and reduced the number andweight of fruit bodies by 2.26-47.2%and 2.19-38.01%, respectively(Sharma and Vijay, 1993).

Symptomatology : Whitishmycelial growth is initially noticedon the casing soil which has atendency to turn greyish yellow. Ifinfection takes place in an earlystage, typical onion shapedmushrooms are produced.Sometimes they appear as small-undifferentiated masses of tissueupto 2cm in diameter. When affectedat later stage, crooked and deformedmushrooms with distorted stipes

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and with tilted cap can be seen.When a part of the cap is affectedharelip symptom is noticed. Affectedmushrooms are greyish in colour. Ifthe infection occurs at later stage,grey mouldy fuzz can be seen on themushrooms. Sometimes littlepustules or lumps appear on the cap.On fully developed sporophores, itproduces localized light browndepressed spots. Adjacent spotscoalesce and form irregular brownblotches. Diseased caps shrink inblotched area, turn leathery, dry andshow cracks. Infected fruit bodiesare malformed, onion shaped andbecome irregular and swollen massof dry leathry tissue (Sharma, 1994).In A.bitorquis, the dark brownblotches caused by V.fungicola varaleophilum are sometimes coveredwith a layer of grey colouredmycelium particularly in the centre.In A.bisporus it causes minorspotting though in variety Les Miz-60 it causes fruit body deformation.An isolate of V.psalliote fromA.bitorquis causes more confluentbrown spots on A.bitorquis but couldnot infect A.bisporus (Zaayan andGams, 1982).

Causal Organism : Verticilliumfungicola

The fungus produces numerousone celled thin walled, oblong to

cylindrical, hyaline conidia, 3.5-15.9x 1.5 - 5u on lateral or terminal,verticillately branchedconidiophores (200-800 x 1.5-5.0 u).Conidiophores are relatively slenderand tall. Conidia accumulate inclusters surrounded by stickymucilage. The fungus abounds insoil.

Epidemiology : Verticillium iscarried on to the farm by infectedcasing soil. Spread is carried out byinfected equipments, hands andclothing. Phorid and sciarid flies arealso known to transmit this disease(Renker and Bloom, 1984). Underlaboratory conditions sciarids andphorids were found to transmit 84-100% and 76-100% of V. fungicolarespectively, into two different media(Kumar & Sharma, 1998). Mites arealso known to transmit the diseasefrom infected to healthy mushroom(Fikete, 1967). The fungus is soilborne and spores can survive in themoist soil for one year. It alsoperpetuates through restingmycelium from dried bulbills and inspent compost. The optimumtemperature for diseasedevelopment is 20C. The periodfrom infection to symptomexpression is 10 days for thedistortion symptoms and 3-4 days forcap spotting at 20C. The pathogengrows best at 24C. However,

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Diseases and Competitor Moulds of Mushrooms and their Management

V.fungicola var aleophilum andV.psalliotae grow best at highertemperature (27C) (Fletcher et al.1986). High humidity, lack of properair circulation, delayed picking andtemperature above 16C favour itsdevelopment and spread (Sohi,1988). It becomes more commonwhen cropping is extended beyond61 days. A number of wild growingfleshy fungi also serve as source ofinoculum. Air borne dust is alsomajor source of primary infectionand may enter houses throughexhaust vents. If infection occursearly, it causes more severemalformation of fruit bodies.Holmes (1971) reported thatinoculum introduced before 21st daycaused low mushroom yield and highdisease incidence. However,inoculum introduced after 14 daysof casing caused the highest diseaseincidence. According to Nair andMacaulley (1987) when crops ofA.bisporus and A.bitorquis wereinfected at casing with V.fungicolavar fungicola and V.fungicola varaleophilum respectively, a relativelyhigh incidence of disease wasobserved but disease was less in thecrops infected at spawning or aftersecond flush. Reduction oftemperature from 20C to 14C andRH from 90% to 80% for 5 days couldnot reduce the severity of the disease.

All the commercial strains aresusceptible (Sharma 1994).However, Poppe (1967) in pot trialsfound brown strain from Francemost resistant to dry bubble disease.

Management

a) Physical methods : Use ofsterilized casing soil, properdisposal of spent compost andproper hygiene and sanitation areessential to avoid primaryinfection (Sharma, 1994). Wuestand Moore (1972) reported thattreating mineral soil with aeratedsteam at 54.4C for 15 minuteseliminated V.malthousi that hadbeen experimently establishedfor 17 days in axenic soil culture.Further in 1973, Moore andWuest reported that thirtyminute treatment with aeratedsteam at 60C and 82C, hinderedspore germination and soilcolonization by V.malthouseimore than similar treatment at98C. Heat treatment of infectedcasing layer at 63C for one hourcompletely prevented sporegermination (Poppe, 1967).

b) Biological method : Accordingto Trogoff and Ricard (1976)spraying casing soil with 100x106

Trichoderma propagules/litre/m2

controlled V.malthousei in

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several trials on naturallyinfected mushroom holdingswhere dry bubble disease wasendemic. Under laboratoryconditions, leaf extracts ofCallistemon lanceolatus,Cannabis sativus, Citrus sp.,Euclyptus sp., Dhatura sp.,Urtica dioica, Solanumkhasianum and Thooja compactacaused 27.77%, 13.05%, 16.66%,22.22%, 5.55%, 6.66%, 22.77%and 27.77% inhibition,respectively of V.fungicola(Sharma and Kumar 1998-99)Bhat and Singh (2000) reported5 bacterial isolates effectiveagainst V.fungicola.

c) Chemical methods : Inlaboratory trials V.malthouseiwas controlled by Zineb on a largescale, Bercema - Zineb 80 used at0.1 - 1.2% controlled the diseasewhen used before and betweenthe flushes (Philipp, 1963).V.malthousei was controlled by 3sprays with Dithane Z-78 at 0.25or 0.50% or Hexathane at 0.30%given at the time of casing, atpinhead formation and afterflushes of crop (Seth et al. 1973).Application of chlorothalonil as adrench reduced the incidence ofV.fungicola tolerant to certainbenzimidazole fungicides.

However, incorporation ofchlorothalonil into the casinglayer caused toxicity to crop anddepressed the yield (Gandy andSpencer, 1976). However, Zaayenand Rutjens (1978) obtained goodcontrol with 2 application ofDaconil 2787 (chlorothalonil) at3g/m2 without any adverse effecton yield. Treatment should beapplied directly after casing andagain 2 weeks later. According toGeijn (1977) disease can becontrolled by spraying withcarbendazim, benomyl orthiophenate methyl at 100, 150and 200g/100m2, respectively in100-150 litres of waterimmediately after casing. Casedbeds can also be treated with 0.5%formalin or 100g carbendazim,150g benomyl or 200gthiophenate methyl in 100-150litres of water per m2 of bed.Zaayen (1979) obtained highestyield with chlorothalonil at 3g/litre water /m2 applied directlyafter casing and again 2 weekslater. Good control of V.fungicolawas achieved by spraying withprochloraz manganese at 60g/100m2 within 7 days of casing andsubsequently at 2 weeksintervals (Fletcher and Hims,1981). Fungicides triadimefon(1g/m2), prochloraz (1g/m2),

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Delsene M (carbendazim +maneb) (8g/m2) andchlorothalonil (2g/m2) appliedafter casing increased the yieldfrom 39.9% in untreated controlsto 56.7, 56.3, 54.6 and 53.1%,respectively (Gandy and Spancer,1981). Zaayan and Adrichem(1982), Russell (1984), Eicker(1987) recommended theapplication prochloraz +manganese complex (Sportak50WP) at 1.5g a.i/m2, 9 days aftercasing. However, only partialcontrol has been achieved byintensive use of prochloraz inSpain (Gela, 1994). Eicker(1984) recommended theapplication of Tecto as drench(450g a.i thiabendazole/dm3) atdosages of 1.838g a.i/m2 aftercasing and 1.44g a.i/m2 betweeneach break. Application ofAmitrole T at 50g, paraquat at10g and diuron at 20-40g after 24hours of inoculation wereeffective against V.malthousei(Popple, 1972). Zaayan and Geijn(1979) suggested new possibilitesfor control of diseases whichadvocated application offormaldehyde (2 litre/100 litresof water/100m3) immediatelyafter casing for effectivemanagement of disease. Ifdisease reappears, replace

formaldehyde by benlate,bavistin, Topsin M throughoutone cultivation cycle. IfV.fungicola becomes resistant tothese fungicides, chlorothalonil(3g /m2) can be used immediatelyafter casing and again 14 dayslater or Curamil (pyrazophos) (at0.5ml/m2) can be applied aftercasing and thereafter at weeklyintervals. According to Flegg(1968) fumigation with methylbromide at a CTP of 600 oz/hr/1000 cu.ft or more can provide asatisfactory alternative to cookout with live steam.

2. WET BUBBLE

Pathogen : Mycogone perniciosa

Common Name : Wet bubble, Lamole, white mould, bubble,Mycogone disease

Wet bubble in white buttonmushroom incited by Mycogoneperniciosa Magn. has been reportedas one of the serious diseases fromalmost all the major mushroomgrowing countries of the world.Bubbles or mole (M. perniciosa),first described from Paris in 1888, isstated to be responsible for theheaviest losses in mushroom beds inFrance, England and United States(Nielson, 1932). The disease has also

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been reported to assume seriousproportions in other majormushroom growing countries of theworld such as United Kingdom,Netherlands, USA, China, Taiwan,South Africa, Brazil, Hungary,Australia and Poland from time totime. In India, this disease wasreported for the first time in 1978from some mushroom farms inJammu and Kashmir (Kaul et al.,1978). Later, this disease has beenreported from the States of HimachalPradesh, Haryana and Maharashtra(Sharma, 1994, Sharma and Kumar,2000, Bhatt and Singh, 2000).

Symptomatology : Many workershave described Symptoms of wetbubble at different stages ofmushroom development. Smith(1924) recognised two mainsymptom types, infected sporophoresand sclerodermoid masses, which heconsidered to be the result ofinfection by M. perniciosa atdifferent stages in the developmentof the sporophores. Thus, wheninfection took place before thedifferentiation of stipe and pileus theselerodermoid form resulted,whereas, infection afterdifferetration resulted in theproduction of thickned stipe withdeformation of the gills (Fletcher andGanney, 1968). Garcha (1978)

described the symptoms in the formof white mouldy growth on themushrooms, leading to theirputrifaction (giving foul odour) witha golden brown liquid exudate. Hsuand Han (1981) reported that theinfected sporophores may berecognised by two symptoms, one istumorous form, infected frompinheads, and other is malformation,infected at later stage. Both types ofinfections may exude water drops onthe surface of infected sporophores.These water drops later change intoamber colour. Tu and Liao (1989)observed that when young pin headsare infected they develop monstrousshapes which often do not resemblemushrooms. Fletcher and Ganney(1969) have reported about 31%infection at the base of the stipe inapparently healthy sporophores inthe form of black streaks. Sharmaand Kumar (2000) described thesymptoms as short, curly, pure whitefluffy mouldy growth of the pathogenon malformed mushrooms, whichcan be easily observed by nackedeyes. Cross section of deformedsporophores without cottony growthshowed black circular area justbeneath the upper layer. Umar etal., (2000) described dramaticcytological changes as a result ofinfection when young (up to 6mm)pin heads were infected. Large, very

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irregular, nodular and tumorousfungal masses are formed and nodifferentiation or organogenesis ofthe cell mass takes place.Mycopathogen grew on the surfaceas fluffy mycelium but was absentdeep on the lesions. TransmissionEM revealed two kinds of cell wallreactions, either focal swelling likecushion at the site of adhesion of M.perniciosa or focal lytic changes withswollen mitochondria.

Nielson (1932) stated that wetbubble caused heaviest losses among

all diseases in mushroom beds inFrance, England and United States.In USA, M. perniciosa was isolatedfrom 3.7 per cent samples collectedfrom various mushroom farms. Forerand his associates (1974) whileestimating the qualitative andquantitative losses caused by wetbubble and dry bubble inPennsylvania (USA), reported thatthese two diseases induced 2.2million lbs. as quanlitative and 19.7million lbs as quantitative loss ofmushrooms. Nair (1977) conducteda survey of 24 mushroom farms in

Symptoms of wet bubble disease

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New South Wales during 1975-76and observed that the mosteconomically important diseases inthese farms include wet bubble.Sharma and Kumar (2000) reportedthat the natural incidence of wetbubble disease of button mushroomranged from 1 to 100 per cent innorthern India. Loss in yield in A.bisporus (S-11) due to this diseaseunder artificial inoculationconditions has been reported to varyfrom 15.72 to 80.13 per cent. Bhattand Singh (2000) have reported theyield loss up to 100 per cent as aresult of artificial inoculation of M.perniciosa.

Etiology : The disease, wet bubble,is caused by Mycogone perniciosaMagn. and the perfect stage isHypomyces perniciosa. Mycelium ofthe pathogen is white, compact, felt-like. Hyphae branched interwoven,septate, hyaline, 3.5m broad.Conidiophores short, slender,branched, hyaline measuring 200 x3-5m and having sub-verticillate toverticillate brances which bear thinwalled, one-celled conidia measuring5-10 x 4-5m. Large two-celledchlamydospores present; upper cellwarty, thick walled, globose, brightcoloured measuring 15-30 x 10-20m,lower cell hyaline, smooth andmeasure 5-10 x 4-5m.

Host Range : Mycogone perniciosa,though a major pathogen of Agaricusbisporus, is also capable of infectingother mushroom species. Figueiredoand Mucci (1985) revealed that M.perniciosa can infect A. campestris.Sisto et al., (1997) have reportedPleurotus eryngii and P. nebrodensissusceptible to M. perniciosa. Sharmaand Kumar (2000) reported all thestrains of A. bisporus (U-3, S-11,791, S-910) and A. bitorquis (NCB-6, NCB-13) susceptible to M.perniciosa under in vivo conditions.

Spread : Spread of M. perniciosaoccurs primarily through casing soilbut the introduction of pathogenthrough other agencies, like spentcompost and infected trash, is notruled out. The infection can be air-borne, water borne or may bemechanically carried by mites andflies (Garcha, 1978). Hsu and Han(1981) reported water splash as animportant factor for wet bubblespread on the beds. Bech et al.,(1982) reported that spread throughcontact occurred readily duringwatering and especially harvesting.They also observed thatcontaminated containers can be asource of spread over greaterdistances. Contrary to other reportsit was also suggested that spores ofM. perniciosa can also be spread by

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air current (Tu and Liao, 1989).Kumar and Sharma (1998) reportedthat transmission percentage of M.perniciosa under in vitro conditions,by sciarid and phorid flies was 100per cent on MEA medium and 4-12per cent on compost.Chlamydospores have been reportedto survive for a long time (upto 3years) in casing soil and may serveas the primary source of inoculum.The aleurospores produced on thesurface of monestrous structures areprobably responsible for secondaryinfection.

Biology / Physiology : Lambert(1930) revealed that Mycogoneperniciosa is quite sensitive toprolonged exposure to moderatelyhigh temperature. The cardinaltemperatures for growth of theorganism on Thaxters agar are 8C,24C and 32C. He also reported thatin agar cultures M. perniciosa waskilled by exposures to temperaturesof 42C (106F) or higher for 6 hr. ormore. According to Zaayen andRutigens (1981) thermal death pointfor M. perniciosa is 48C. Bech andKovacs (1981) reported that aqueoussuspension of Mycogone spores canwithstand 42C and 36C for 10minutes and 1 hr, respectively. Hsuand Han (1981) reported thatoptimum temperature for mycelialgrowth, sporulation and conidial

germination was 25C. He alsorecorded pH 6.0 as optimum forconidial germination. According toLiao (1981) chlamydospore failed togerminate on various media in vitroeven after heat (40-70C) treatmentor application of chemicals andsolvent. However, germinationoccurred on potato dextrose agar(PDA) medium exposed to the gasproduced by mushroom mycelia incompost for 36 hrs at 24C. In anthorstudy Bech and Kovacs (1981) foundthat aleurospores are unable togerminate in water, Richardssolution, pressed mushroom juice orin PDA but verticilloid sporesshowed a certain degree ofgermination in diluted mushroomjuice and on PDA. As reported by Tuand Liao (1989) the pathogen istolerant to a wide pH range in acidside and able to grow at pH 4.4,however, the growth becomesweaker or rather restricted at pH 8.4.Holland and Cooke (1991) reportedthat in malt extract agar medium M.perniciosa formed abundant thinwalled, hyaline phialo conidia andthick walled pigmented verrucoseconidia. During nutrient deplectionother propagules appeared, namely,lateral smooth conidia, infectedinterculary cells, chlamydosporesand arthro conidia. Singh andSharma (2000) have reported themaximum growth of M. perniciosa

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on PDA. Optimum temperature andpH for growth were reported to be25C and 6.0, respectively. Mannoseand asparagine have been reportedas best sources of carbon andnitrogen, respectively. Sharma andKumar (2000) observed compostextract agar medium as the best forthe mycelial growth and malt extractpeptone dextrose agar medium forspore production. A pH range 5-6was found optimal for the mycelialgrowth.

Management : As the pathogeninflicts serious damage to the crop,various attempts have been made tomanage the disease through variousmeans.

a) Physical : Wuest and Moore(1972) suggested that aeratedsteam at 54.4C for 15 minutescan eliminate M. perniciosa fromcasing soil. Munns (1975)suggested the use of plastic potsto cover mushroom showing wetbubble symptoms during thecropping season to prevent spreadof disease. Tu and Liao (1989)while working to find out anintegrated approach for themanagement of wet bubbledisease revealed that the use ofclean compost, pasteurization orsterilization of casing soil, goodpeak heating and fumigation of

mushroom house and use ofbenomyl or Mertect 40 per centwere effective in managing M.perniciosa. Zhang (1990)suggested three methods ofprevention of wet bubble diseasewhich include steam sterilizationof mushroom beds, formaldehydefumigation and fungicidalapplication. Another method likescreening and selection of diseaseresistant strains should also beexploited.

b) Biological : Jhune et al., (1990)screened 12 isolates of bacteriaand 71 isolates of actinomyectesisolated from mushroom compostand casing mixture and observedAJ-117, AJ-136 and AJ-139 aspromising bioagents. Though,almost negligible attempts havebeen made to control M.perniciosa through botanicals butthe inhibition of fungal growth byplant extracts is not uncommonand has been reported earlier bya number of workers (Flierman,1973; Michal and Judith, 1975).Gandy (1979) made aninteresting observation thatAcremonium strictum produces aheat stable antibiotic compoundpossibly a cephalosporin, whichis inhibitory to M. perniciosa butno attempts have been made toexplore this approach as both

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fungi are pathogenic tomushrooms.

c) Chemicals : Benomyl spray at0.5-4g/m2 immediately aftercasing has been reported veryeffective for protecting the crop(Gandy, 1974; Stanek andVojtechovska, 1972). Fletcher(1975) advised that adequatecontrol of wet bubble wasobtained by benomyl orThiophanate methyl at 10g a.i. atcasing while TBZ was lessaffective. Kim (1975) recordedsatisfactory control of wet bubbleby spraying benomyle @ 0.5g a.i/m2 , 3 days after casing. Geijn(1977) suggested the control ofwet bubble disease by sprayingthe crop with carbendazim,benomyl or thiophanate methylat 100-150 litre waterimmediately after casing.Basamid (Dazomet) and Vapam(Metham sodium) applied @100ppm to casing has also beenreported very effective (Kim etal.,1978). Application ofcarbendazim, benamyl,chlorothalonil, TBZ, prochlorazmanganese complex (Sportak 50WP) into casing mixture havebeen reported very effective forthe management of wet bubble byseveral workers (Hsu and Han,1981, Zaayen and Adrichem,

1982; Fletcher, 1983; Zaayel etal., 1983; Eicker, 1984; Jhune etal., 1991; Sharma and Kumar,2000). It was reported that ifcasing is contaminated controlcan be achieved by treating itwith 1 per cent formalin.Alternatively, a spray of 0.8 percent formalin on to casingsurface, immediately after casing,can be effective. However, thisconcentration can be injurious ifused at a later stage in cropdevelopment. Sharma et al.,(1999) have reported 62.5-100per cent inhibition of M.perniciosa in culture wheninoculum discs were drenched in0.5-2% formalin solution for 5seconds. Exposure of M.perniciosa cultures to vapours of1-4 per cent formalin for 6-24 hrsalso resulted on 100 per centinhibition of fungal growth onsub-culturing.

3. COBWEB

Pathogen : Cladobotryumdendroides

Common Name : Mildew, Softdecay, Hypomyces mildew disease,Dactylium disease.

This disease renders extensivedamage either by causing soft rot or

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decay of fruiting body. Merat (1821)described this disease as Botrytisdendroides and transferred it in tothe genus Cladobotryum by makinga combination C.dendroides (Bull :Merat) W.Gams et Hoozem. Salmanand Ware (1933) were the first toreport D.dendroides being parasiticto mushrooms. According toFletcher and Atkinson (1977)mushroom of any age of developmentwould be attacked by this fungus.This disease causes great damage tomushroom houses where humidityis high (Bozhkor, 1975). Forer et al.(1974) isolated C.dendroides from0.6% of mushroom sampled fromcommercial mushroom houses inPennsylvania. In India it was firstrecorded in Chail and Shimla (HP)(Seth, 1977) and later from Solanand Kasauli with natural incidenceranging from 8.17 - 18.83% in 1982and 1.93-25.63% (Seth and Dar,

1989). Under artificial inoculationconditions with different levels ofinocula, the loss in marketablemushrooms has been estimated at66.6% (Sharma and Vijay, 1996) and21.95 - 48.95% at differenttemperatures (Seth and Dar, 1989).Sharma et al. (1992) recordedC.verticillium a new pathogen ofA.bitorquis in Himachal Pradesh.

Symptomatology : Cobwebappears first as small white patcheson the casing soil which then spreadsto the nearest mushroom by a finegrey white mycelium. A floccosewhite mycelium covers the stipe,pileus and gills, eventually resultingin decomposition of entire fruit body.As the infection develops, myceliumbecomes pigmented eventuallyturning a delicate pink cover (Laneet al. 1991). In severe attacks, adense white mould develops over

Symptoms of cobweb

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casing and mushrooms change froma fluffy cobweb to a dense mat ofmycelium. The white colour canturn pink or even red with age. Onesymptom which can appear andwhich is generally not associatedwith the disease is cap spotting. Thespots can be brown or pinkish brown(Sharma, 1994). On inoculated fruitbodies, characteristic symptomsappeared within 24 hours ofinoculation when mycelial + sporesuspension were applied, symptomsappeared 4-12 days after infestation.Younger mushrooms are moresusceptible than fully developedones. Tuffs of conidiophers developon all sides of the web and growth ofengulfed mushroom is arrested. Onremoval of mycelial felt from affectedmushroom, drops of dark browncoloured fluids exudes emittingbitter foul smell (Seth and Dar,1989).

Causal organism : Cladobotryumdendroides (Dactylium dendroides)imperfect state of Hypomycesrosellus. Sterile hyphae form a turfand are prostrate, branched, septateand hyaline with approximatelyopposite branches, which divideabove into usually three pointedbranchlets. Conidiophers are erect,similar or branched in many whorls.Conidia single, elongate pointed atthe base, 2-3 septate, slightly

constricted at the septa and measure20-30 x 10-12.5 u. It produces sexualstage belonging to Hypomycesrosellus, which has been observed ondecaying dried fruit bodies of wildmushrooms in HP.

Epidemiology : High relativehumidity and temperatureencourage the disease. Spread ismainly by conidia. The pathogen isa soil inhabiting fungus and isnormally introduced into the crop bysoil contamination, spores,mycelium on crop debris or by farmworkers. Spores are easily spread byair movement, workers hands, toolsand clothing and by water splash(Sharma, 1994). Under laboratoryconditions, sciarids and phorid flieswere found to transmit 4-100% ofthe disease in to two different media(Kumar and Sharma, 1998). A highRH and temperature range of 19-22C and 12-15C resulted inmaximum loss in yield (Seth andDar 1989). Optimum temperaturefor growth is 20C and for sporegermination is 25C. C.dendroideshas been isolated from woodland soil(Canada) moss (Polytrichum sp.)(UK), a bracket fungus Stereum sp.(UK), dead wood (Pinus sp.) andmushroom farms (Lane et al. 1991).On the other hand disease caused byC. verticillatum on A. bitorquis wasfavoured by RH 90% and

14


temperature of 25-30C (Sharma etal., 1992).

Management

Physical : Through disinfection ofcasing soil with live steam orsterilization of casing mixture at 50Cfor 4 hours effectively eliminates thepathogen. Regular cleaning, removalof cut mushroom stems and younghalf dead mushrooms after eachbreak and controlling temperatureand humidity helps in controllingthe disease (Sharma, 1994).

Biological : Under laboratoryconditions, leaf extract of Cannabissativus, Ricinus cummunis,Callistemon lanceolatus, Citrus sp.,Euclyptus sp., Dhatura sp. andUrtica dioica were found to cause5.55%, 10.55%, 18.55%, 26.11%,34%, 19.07% and 23.33% inhibitionof C.dendroides (Sharma andKumar, 1988).

Chemical : Terraclor(pentachloronitrobenzene) caneradicate Dactylium mildew evenafter the well establishment of thedisease (Stoller et al., 1956).Bozhkor (1975) suggested annualdisinfection of houses andsurrounding areas with 2%bordeaux mixture or with 5%formation solution at 0.5-1.0 l/m2 or

fumigation with 2.0-2.5 l formationands 0.5-1.0 kg chlorinated lime/100m3 for controlling disease. He furthersuggested that immediate spray aftercasing with benomyl at 1g in 0.5 -1.0l water/m2 also controls the disease.According to Russell (1984) singleapplication of prochloraz manganesecomplex (sporogon) at 1.5g a.i./m2 ofbed 9 days after casing givessatisfactory control of the diseases.Seth and Dar (1989) obtained bestcontrol of disease by applyingbavistin + TMTD at 0.9 and 0.6g/m2

followed by TBZ and benlate (0.9g/m2). Effective control of C.verticillatum was obtained byspraying with 0.05% carbendazim atspawning followed by 0.25%mancozeb at casing and carbendazimagain 15 days later (Sharma et al.1992).

4. GREEN MOULD

Pathogen : Trichoderma viride, T.hamatum, T. harzianum, T. koningii,Penicillium cyclopium, Aspergillusspp.

Common names : Trichodermaspot, Trichoderma blotch,Trichoderma mildew, Green mould

One of the most common anddestructive diseases in mushroomcultivation is the green mould which

15


is mainly caused by different speciesof Trichoderma, Penicillium andAspergillus. Among these moulds,Trichoderma spp. induce significantquantitative and qualitative losses inthe yield of Agaricus bisporus,Pleurotus spp., Auricularia,Calocybe indica and Lentinulaedodes. Kligman (1950) was the firstto report the presence ofTrichoderma in mushroom compost.Different species of Trichodermawhich have been reported ascompetitors and / or pathogenic onbutton mushroom include, T. viride,T. koningii, T. hamatum, T.harzianum, T. atroviride, T.pseudokoningii, T. logibrachiatum.Among all these species, T.harzianum is recognised as causingthe most severe problems (Morris etal., 1991; Seaby, 1996). Seaby (1989)recorded 9 distinct groups ofTrichoderma species and strainswhich had almost similar sporebearing structures as described byRafai (1969). These included, T.viride, T. harzianum (Th-1, Th-2,Th-3), T. koningii, T. pseudokoningiiand T. longibrachiatum. Geneticallydistinct biotype Th-4 of T.harazianum has been responsiblefor serious outbreak in USA. InIndia, T. viride was first reported byThapa and Seth (1977) on A.bisporus, and T. hamatum and T.

harzianum by Seth and Bhardwaj(1986-87).

Economic Importance : Greenmoulds caused by Trichodermaspecies were once recognised asindicators of poor compost qualityand were of minor significance. Thedevastating nature of T. harzianumwas undocumented in mushroomindustry until 1985 when it was firstobserved in Ireland and resulted inlosses estimated at 3-4 millionpounds to the U.K. and Irishmushroom industries. The secondwide spread epidemic occurred inearly 1990s in Ireland (Seaby, 1996).Green mould epidemics have beenreported from the USA, Canada,South America, Asia, Australia andEuropean countries. T. harzianumbiotype Th-2 was responsible forsevere epidemics in Europe andbiotype Th-4 in America (Mamounet. al., 2000). Crop losses to greenmould are variable, however, sincethe onset of the disease inPennsylvania crop losses have beenestimated in excess of $30 million(Anderson et al., 2000). Yield lossesin first flush of A. bisporus byartificial inoculations have been upto 8% for T. pseudokoningii and 26%for T. atro viride (Grogan et al.,2000). Sharma and Vijay (1996)have reported yield loss in A.

16


bisporus from 12.5-80.8% by artificialinoculation of T.viride at differentinoculum loads and at differentstages of crop growth. Jandaik andGuleria (1999) reported 5-46.87%and 6.25-50.0% yield losses due to T.viride and T. harzianum,respectively under artificialinoculation conditions. Anderson etal., (2000) recorded significantdifferences among hybrid mushroomstrains in response to T. harzianumbiotype 4 (Th-4) infestation. Hybridwhite strains were the least resistantto green mould, sustaining yieldlosses upto 96%. Hybrid off-whitestrains exhibited intermediate

susceptibility with yield losses of 56-73%. Brown strains weresignificantly resistant to greenmould, sustaining yield losses of only8-14%.

Symptomatology : Differentspecies of Trichoderma have beenreported to be associated with greenmould symptoms in compost, oncasing soil, in the spawn bottles andon grains after spawning. A dense,pure white growth of mycelium mayappear on casing surface or incompost which resembles tomushroom mycelium. Later onmycelial mat turns to green colour

Symptoms of green mould

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because of heavy sporulation ofcausal agent which is a characteristicsymptom of the disease. Thereafter,the mould creeps to surface of casinglayer and infects the new parts anddeveloping newly borne primordia.Mushrooms developing in or nearthis mycelium are brown, may crackand distort, and the stipe peels in asimilar way to mushrooms attackedby Verticillium fungicola causing drybubble disease. Some species inducebrownish lesions / spots on capswhich may cover the entire capsurface under congenial conditions.

Causal organism : Several speciesof Trichoderma are associated withgreen mould disease complex of A.bisporus. The taxonomy of thisgenus has caused confusion and asuccession of mycologists haveinvestigated it since the turn of thecentury. In 1939, A. R. Bisbyreviewed the literature andconcluded that although there weredifferences in morphology betweentypes these were not consistent anddistinct. He, therefore, classified alltypes as T. viride whilst recognizingthat considerable but inconsistentvariability existed. In 1969, Rifairevised the genus and proposed ninespecies aggregates. His classificationis now the one that is generallyaccepted. The species recorded inmushroom culture include T. viride,

T. harzianum and T. koningi. T.viride is said to be weed mould, T.koningi a pathogen whilst T.harzianum has been ascribed to avariety of roles including pathogenand agent for biological control. Fourbiotypes namely, Th-1. Th-2, Th-3,and Th-4 have been furthercharacterized in T. harzianum onthe basis of occurrence, symptoms,morphological characters andphysiological requirements (Seaby,1989).

T. viride (T. lignorum) : This iswidespread in soil. Spore are ovoid,rough walled, green and measure2.8-5x2.8-4. The colony emitscoconut odour. This fungus grewslowly at 27C but faster at 20C.

T. koningi : This is commoninhabitant of soil. Spores are smoothwalled, cylindrical, green andmeasure 3-4.8x1.9-2.8m. Colonyemits no odour. Spores germinatefaster than other species and growthrate is 1-1.2mm/hr.

T. harzianum : Common in soils.Colonies growing rapidly, mostisolates 7-9cm in diameter after 3-4days, aerial mycelium floccose, whiteto greyish. Conidiation on MEAinitially as compact and produce aflat postule often concentric that isgreen whitish and later turn to dark

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green colour. Chlamydospores fairlyabundant, intercalary or terminal,solitary, smooth walled, mostly 6-12mm. in diameter. Macronematousconidiophores highly branched.Conidia smooth walled, ovoid, greenin colour and measure 2.4-3.2x2.2-2.8m. Four biotypes, Th-1, Th-2, Th-3 and Th-4 have been furthercharacterized in T. harzianum onthe basis of morphological, cultural,physiological and geneticalvariations.

Epidemiology : Green mouldgenerally appears in compost rich incarbohydrates and deficient innitrogen. If the compost is tampledtoo hard in the beds, or the fillingweight is too high, this can make thepeak heating difficult. This iscertainly the case with compostwhich has a short texture and whichmight also have too high moisturecontent, resulting in improperpasteurization and conditioning ofcompost. Frequent use of formalinalso tends to promote thedevelopment of green moulds(Sharma et al., 1999). Differentsources of primary inoculum ofTrichoderma spp. could be dustparticles, contaminated clothings,animal vectors especially the mite,Pygmephorus mesembrinae, miceand sciarid flies, air-borne infection,infected spawn, surface spawning,

contamination of compost byhandling and machinery andequipments at the mushroom farm(Seaby, 1987). Spore concentrationless than 1x102 was unable to causeinfection (Grogan et al., 2000).Benomyl treated grain spawn orcompost spawn in normal composthad less T. harzianum. High relativehumidity accompanied by a low pHin the casing soil also promotes thedevelopment of Trichoderma spp.(Sharma and Jandaik, 1999).Chlamydospores produced by T.harzianum, T. viride, T.longibrachiatum and T.pseudokoningii survived theexposure of 9 hours at 60C (Morriset al., 2000). T. harzianum inducedsignificant yield reductions at 30Cthan at 20C (Seaby, 1986).

Control : Green moulds can beprevented by

a) Very good hygiene

b) Proper pasteurization andconditioning of compost.

c) Sterilizing the supplementsbefore use and mixing themthroughly preferably afterspawning.

d) Using the correct concentrationof formalin (maximum 2%)

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e) Weekly sprays of mancozeb(0.2%)or bavistin (0.1%) TBZ(0.2%) ortreatment with zineb dust orCalcium hypochlorite (15%) havegiven effective control of thedisease.

b. Competitor moulds

5. FALSE TRUFFLE

Pathogen : Diehliomyces microsporus

Common name : Truffle disease

This is the most dreadedcompetitor in mushroom beds. It wasfirst reported by Lambert (1930)from Ohio, USA during 1929 anddescribed by Diehl and Lambert(1930) as Pseudobalsamiamicrospora. Glasscock and Ware(1941) observed it in UK and studiedits invasion in mushroom beds.False truffle incidence in theNetherlands was reported by Bels-Koning and Bels (1958) but itsserious incidence was noticed in thecrops of Agaricus bitorquis, grown athigher temperature (Zaayen and Pol-Luiten, 1979). Gilkey (1954)reclassified the fungus fromTuberales to the Eurotiales andnamed the genus Diehliomyces. InIndia, Sohi et al. (1965) observedfalse truffle causing serious losses tomushroom crops when the compost

temperature in the trays reachedbeyond 22-24C. The naturalincidence of false truffle in A.bisporus grown under naturalclimatic conditions has been reportedfrom 1-80% in the States ofHimachal Pradesh, Haryana, Punjaband Uttar Pradesh (Sharma andVijay, 1996). False truffle is a limitingfactor in the production of A.bitorquis in India because of itshigher temperature requirements.The disease is of common occuranceduring February or early March inA. bisporus in the plains of theNorthern India and during summermonths in A. bisporus and A.bitorquis in hilly regions of thecountry. Sharma and Jandaik (1996)reported 66-88 per cent incidence ofthis competitor in Himachal Pradeshduring 1993-1996 resulting in 58-80% yield loss.

Symptoms : The coulour of thefluffy mycelium is white to start withand turns a creamy yellow at a laterstage. It appears as small wefts ofwhite cream coloured mycelium incompost and casing soil, usuallymore conspicuous in the layer wherecompost and casing mixture meetand also on casing. Gradually themycelial growth become thicker anddevelops into whitish, solid,wrinkled, rounded to irregularfungal masses resembling small

20


brains (ascocarps of the fungus),looking like peeled walnuts. Theyvary appreciably in size ranging from0.5 to 3cm in diameter. At maturitythey become pink, dry and reddishand finally disintegrating into apowdery mass emitting a chlorinelike odour. The fungus does notallow the mushroom mycelium togrow and compost turns dull brown.The spawn in affected patches turnssoggy and disappears.

Causal Organism : Diehliomycesmicrosporus (Diehl and Lambert)Gilkey, ascocarps are formed fromthe dense tangled hyphal knotssingly or several knots coalesce toform large ascocarp. Ascocarps arefleshy, at first white then brownishand finally reddish brown containingnumerous sac like asci which areoval, sub-spherical, short or long-stalked, with 3-8 ascospores, 19-27x10.5-15m. Ascospores are

spherical, sulphur coloured with onedistinct oil drop and measure 6.5min diameter. Chlamydospores may benoticed in the hyphal web ofascocarp.

Epidemiology : Ascosporesdevelop in the truffles in 3 to 6 weeksand are released when the truffledisintegrates. Ascopore productionis abundant at 25 and 30C but notat 15 or 37C (Wood and Fletcher,1991). Ascopore germination upto70% has been recorded at 27C aftergiving heat stimulus at 40-50C forhalf an hour. (Zaayen and Pol-Luiten; Sharma 1998). The majorsources of infection are casing soiland surviving ascospores/myceliumin wooden trays from the previouscrops. Ascopores can survive for aperiods of 5 years in soil and spentcompost and mycelium for 6 months(Sharma, 1998) and thus serve as themajor source of primary inoculum.

Symptoms of false truffle

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Stage of infection and temperatureare important factors fordetermining the severity of thedisease. Optimum growth of thefungus has been recorded at 26-28C.False truffle seems to depend eitheron mushroom metabolities or ondepletion of inhibitory factor bymushroom mycelium. It is mainly adisease of A. bitorquis wherein cropis raised at 251C but it alsodevelops very fast in A. bisporuswhen crop is taken under naturalclimatic conditions and temperaturerises above 20C.

Control

1. Compost should be prepared ona concrete floor and never onuncovered soil. Because duringcomposting there is rise intemperature which activates theascospores present in the soil.

2. Pasteurization and conditioningof the compost should be carriedout carefully. Maszkiewiez andSzudyga (1999) observed thatpasteurization of compost underoptimum condition completelyeliminated the false truffleincolum in the compsot.

3. Temperature above 26-27Cduring spawn run and aftercasing should be avoided. During

cropping, temperatures shouldbe kept below 18C . Under suchconditions, it is practicallyimpossible to grow A. bitorquisbut disease can be managedeffectively in A. bisporus.

4. Casing soils known to harbourtraces of spores should not beused. Young truffles must bepicked and buried before the fruitbodies turn brown and spores areripe.

5. Woodwork, trays or side-boards ofshelf-beds should be treated witha solution of sodium-pentachlorophenolate at the endof the crop which was infectedwith the truffle disease. Air-drying of wood-work for 2-3months may also eradicate thepathogen.

6. Good cooking out (composttemperature 70C for 12h.) atthe end of the crop should becarried out which will killmycelium and spores of thepathogen in the compost.Wooden trays should beseparately chemically sterilized.Thermal death point ofascospores and mycelium hasbeen reported to be 70C for 1hr. and 45C for 30 minutes,respectively (Sharma, 1998).

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7. Initial infection can be checkedby treating the affected patcheswith formaldehyde (2%) solution(Sohi, 1988).

6. OLIVE GREEN MOULD

Pathogen : Chaetomium olivaceum,C. globosum

The first evidence of theoccurrence of C. olivaceum in Indiawas provided by Gupta et al., (1975)at the mushroom farm at Chail,Kasauli and Taradevi. Anotherspecies, C. globosum, was laterreported from mushroom farms inHP, Delhi and Mussorie (Thapa et al.,

1979). Yield losses ranging from12.8-53.65% have been reported inA. bisporus (Sharma and Vijay,1996).

Symptoms : The earliest signs ofthe fungus consist of aninconspicuous greyish-white finemycelium in the compost or a fineaerial growth on the compost surface10 days after spawning. Frequentlyinitial spawn growth is delayed andreduced. By late spawn run, fruitingstructures that look like gray-greencockle-burns-1/16 inch in diameter,develop on straw in isolated spots ofthe affected compost. The compostwill have a musty odour. Compost

Symptoms of olive green mould

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not supporting spawn growthgenerally supports the growth ofChaetomium and other severalmoulds and hence olive green mouldis not the exclusive colonizer of blackcompost. Spawn usually grows intoareas occupied by Chaetomium,although normal spawn growth isdelayed. C. globosum is also noticedon spawn bottles.

Causal organism : Chaetomiumolivaceum Cooke and Ellis, C.globosum Kunze ex Steudel

The fungus consists of a grayishwhite mycelium which laterproduces perithecia. Perithecia of C.olivaceum are superficial, opaque,globose, thin, membranous with anapical tuft of dark bristles of setae.Asci clavate and evanescent.Ascospores dark brown, broadlyovoid, umbonate at both ends andmeasure 9-12.5x7-9.5m. Peritheciaof C. globosum are scattered orgregarious, broadly ovate or ellipsoid,often pointed at the base, thickly andevenly clothed with slender flexuoushairs. Asci oblong-clavate andevanescent. Ascospore dark, broadlyovoid, faintly apiculate at both endsand measure 8-9.5x6-8m.

Epidemiology : The infectionusually comes through air, compost

and casing soil. It appears due todefective composting in phase-IIbecause of improper pasteurizationaccompained by high temperaturesin the absence of adequate fresh air.Improper stacking of the composttrays in the pasteurization roomwhich do not allow proper circulationof the air or overfilling of the roomcauses intensive condensation whenwet steam is introduced, result innon-selective compost whichharbours Chaetomium and othermoulds. Spores are resistant to heatand are probably not killed easilyduring pasteurization. It is also wellknown that spores of Chaetomiumare already present in the compost(Munjal et al., 1977, Sharma, 1992)which are activated by bad peakheating control. When compost is toowet, penetration of air is less whichresults in the conversions ofnitrogenous compounds in wrongdirection. Unfavourable conversionsoften results in renewed productionof anhydrous ammonia whichprompts the growth of ammonia.Sometimes the temperature is toohigh in certain spots of a room, ormay be less of oxygen which oftenresults in olive-green mouldappearance. Ascospores are spreadby air flows, clothes and othermaterials used in mushroom farm.

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Control

1. The fermentation period of thecompost should not be too short.It is essential to provide an activecompost that is not too wet andhas a good structure.

2. Do not add nitrogen, ammoniumsulphate, urea, chicken manureor similar materials just beforefilling.

3. There should be sufficient timefor peak-heating and sufficientsupply of fresh air duringpasteurization. Highertemperatures (above 60C) forlonger time should be avoided.

4. Large number of fungicidesincluding Benomyl, Thiophanatemethyl, TBZ, Vitavax, DithaneZ-78, Dithane M-45, Thiram andCaptan have been found effectiveunder in-vitro conditions (Thapaet al., 1979) and sprays ofDithane Z-78 (0.2%) have beenrecommended for checking thesecondary spread (Sohi, 1986).

8. BROWN PLASTER MOULD

Pathogen : Papulaspora byssinaHots.

Papulaspora byssina was firstreported on horse dung compost

from Missouri (Hotson, 1917).Charles and Lambert (1933) laterreported its occurrence onmushroom beds and recordeddelayed yields in the presence of thismould. This disease has also beenreported from India (Munjal andSeth, 1974) causing 90-92% yieldloss in A. bisporus. This mould hasalso been reported to cause completecrop failure in oyster mushrooms inKasuali, HP (Dar and Seth, 1981).This fungus now is frequently foundat almost all the mushroom farms inIndia appearing usually duringspawn run (Garcha et al. 1987; Kaulet . al. 1978; Sharma, 1992). Thismould has invariably been isolatedfrom different compost and casingsamples collected from mushroomfarms in northern India and theincidence of the disease has beenrecorded from 5 to 9%. (Sharma andVijay, 1996). Loss in number andweight of fruit bodies as a result ofartificial inculation of the mould hasbeen found 7.7-53.5% and 3.0-50.7%respectively (Sharma, 1990; Sharmaand Vijay, 1993).

Symptoms : It is first noticed aswhitish mycelial growth on theexposed surface of compost andcasing soil in trays as well as on sidesin bags due to moisturecondensation. This develops furtherinto large dense patches gradually

25


changing colour through shades oftan, light brown to cinnamon brown;ultimately becoming rust coloured.No mushroom mycelium grows onplaces where plaster mould occurs.

Causal Organism : Papulosporabyssina

The mycelium is brownish,septate; later produces clusters ofbrown coloured many celled,spherical bulbils measuring 60-130x30-190. These are inter-wovenwith a net work of hyphae, are setfree later with the death of themycelium.

Symptoms of brown plaster mould

Epidemiology : Primary infectioncomes through air-borne bulbils orcontainers, compost and casing soiland workers. Its development isfavoured by wet, soggy and wronglyprepared compost. Highertemperature during spawn run andcropping favours the diseasedevelopment. In wet, greasy compostwhich had not received enoughoxygen during fermentation andmany of amines, development of thedisease is greatly favoured. Additionof less quantity of gypsum and moregreasiness favour the diseasedevelopment.

26


Control

Composting should be carriedout carefully, using sufficient gypsumand not too much water. Peak heatingshould be of sufficient duration andat proper temperatures. Thecompost should not be too wet beforeor after peak heating.Munjal andSeth (1974) recommended localizedtreatment of infected patches with2% formalin while Seth andShandilya (1978) recommended 4%formalin for its control.Largenumber of fungicides namely,benomyl, carbendazim, thiophanatemethyl, vitavax, daconil, MBC,dithane Z-78, dithane M-45, captan,thiram and copper fungicides havebeen screened under in vivo and invitro conditions by various workers(Thapa et al. 1979; Kaul et al.,1978; Dar and Seth, 1981). Sprayingof systemic fungicides at 0.1%concentration has also beenrecommended.

9. YELLOW MOULD : (Matdisease; Vert-de. gris)

Pathogen : Myceliophthora lutea,Chrysosporium luteum, C.sulphureum

All these fungi produce yellowmycelial growth in the compost.Constantin (1892) reported M. lutea

from French mushroom caves for thefirst time. Yellow mould inducingmat disease has been reported fromJammu & Kashmir (Kaul et al.,1978), Punjab (Garcha et al., 1987)and Himachal Pradesh (Thapa &Seth, 1986-87; Seth & Bhardwaj,1989) inducing 5-20% loss on theyield of button mushrooms undernatural conditions. Artificialinoculations with M. lutea atdifferent stages caused 27-89% lossin yield. The incidence of the diseasein HP has been reported from 20-60% during 1981-83 and 10-70%during 1985-86. Recently, thedisease has also been noticed inDistt. Sonepat in Haryana State.

Symptoms : The yellow mouldsmay develop in a layer below thecasing (Mat disease), form circularcolonies in the compost (confetti) orthey may be distributed throughoutthe compost (Vert-de-girs). In India,M. lutea has been reported to inducemat disease. This fungus forms ayellow brown corky mycelial layer atthe interphase of compost and casingwhich is difficult to detect during theimpregnation of casing layer by thespawn and even during the firstbreak. It becomes apparent when itdevelops its stroma like morphologyand mushroom production isseverely inhibited.

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Causal organism :Myceliophthora lutea

The mycelium is whitish at firstthen yellow to dark tan withrestricted growth and creamish ordull white sporulation. Hyphaeseptate, hyaline, branched. Itproduces three kinds of spors, (i)Smooth, ovoid terminal condia bornesingly, (ii) Smooth, thick walledchlamydospores, terminal orintercalary and (iii) thick walledspiny chlamydospores.

Epidemiology : The major sourcesof primary inoculum are air, chickenmanure, spent compost anddefectively sterilized wooden trays(Seth & Bhardwaj, 1989).Thesecondary spread is mainly throughmites followed by flies, watersplashes, picking and tools. The

fungus survives easily through thickwalled chlamydospores. Diseaseseverity is generally more at 70%moisture content of the compost and19-20C temperature.

Control

1. Proper pasteurization of thecasing mixture is very essential.Fungus does not survive theexposure for 6 hrs. at 51C or 4hrs at 54C.

2. Benomyl (400-500ppm) andblitox (400ppm) sprays havebeen found effective to controlthe disease and increase the yield(Seth and Bhardwaj, 1989).Spraying with calciumhypochlorite solution (15%) iseffective for eradication of themould growth (Sohi, 1986).

Symptoms of yellow mould

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10. SEPEDONIUM YELLOWMOULD

Pathogen : Sepedonium spp.

Yellow mould disease induced bySepedonium has been reported inIndia by Thapa et al., (1991) and theincidence of the mould has beenreported by vary from 5-20% withinsignificant reduction in yieldexcept in extreme cases. One morespecies, S. maheshwarinum, has alsobeen reported by Vijay et al., (1993)with very high incidence causingsevere losses or even complete cropfailures. Bhatt and Singh (2000)have recorded 1.6 to 8% incidence ofyellow mould in Haryana and UPStates and 32 to 64% loss in yieldunder artificial inculations.

Symptoms : This mould is mainlyobserved in the compost and isinitially white in colour turning toyellow or tan at maturity. It isgenerally present in the lower layersof the compost or at bottom of thecropping bags. Various types ofdistortions in fruit bodies arecommonly observed, probably due tothe production of volatile substancesor toxins. These toxins inhibit thespawn and ultimately mushroommycelium disappears from thecompost.

Causal organism : Sepedoniumchrysosporium (Bull.) Fries., S.maheshwarianum Muker.(Hypomyces chrysosporium Tull.)

Mycelium is white initially,turns yellow to tan with age.Hyphae septate, brenched, hyaline,moderately thick, 3-5mm wide.Conidiophores erect, bear lateralsimple or botryose cluster ofbranches, 4-4.5mm wide, usuallyseptate, bearing spores singly andterminally on the branches. Twotypes of spores are produced inlarge numbers. Conidia arehyaline, thin walled, ellipsoid orpyriform, produced singly from thetips of the phialids. Second type ofspores are like chlamydosporeswhich are globse, warted, darkyellow, thick walled and 13-21mmin diameter.

Epidemology : Primary source ofinculum are probably, soil, spentcompost, air or improperly sterilizedwooden trays. The chlamydosporeare thick-walled and resistant to heatand in this spore form, the fungusmay survive peak-heat. Spores canbe spread to the compost by aircurrents prior to or during fillingoperation, during the spawningoperation or with unpasteurized orspent compost sticking to wooden

29


trays. Conditions favourable forbutton mushroom cultivation alsofavour the Sepedonium mould.Higher N content, especially in theform of chicken manure, have beenreported to favour the moulddevelopment (Vijay et al., 1993). Itsappearance in the lower layers of thecompsot has been linked with morewetness. Sharma and Sharma(2000) have reported very highpopulation of Sepedonium spp. in3-12 months old chicken manurewhich may serve as the primarysource of inoculum in long methodof compost.

Control

Strict temperature monitoringand control during compostpasteurization and an adequatepost-crop cooking out are essentialto eliminate the threat ofinfestation. Preventing the entry ofspores during spawning andspawn-running by installing high-efficiency air filters are essential.Incorporation of 0.5% carbendazimin compost and sterilizing thechicken manure (for long methodof composting) with 2% formalinand 0.5% carbendazim has givengood results (Vijay et al., 1993).

11. INK CAPS

Pathogen : Coprinus spp.

Common names : Ink weed, wildmushrooms

The appearance of inky capsduring spawn run is commonlyobserved on the mushroom beds innorthern India (Kaul et al., 1978;Garcha 1984; Sohi, 1986). Artificialinculations of C. fimetarius atdifferent loads of inoculum atspawning has resulted in 20.14-94.4% reduction in the number offruit bodies and 14.68 to 94.43%reduction in the weight of fruitbodies (Sharma 1992).

Symptoms

Ink caps appear in the compostduring spawn run or newly casedbeds and outside the manure pilesduring fermentation. They areslender, bell-shaped mushrooms.Cream coloured at first, blueish-black later and are usually coveredwith scales. This fungus sometimesgrows in clusters in beds and has along sturdy stem which oftenreaches deep into the compost layer.Several days after their appearanceink caps decay and form a blackishslimy mass due to autodigestion.

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Causal organism : Coprinusatramentarium, C. lagopus, C.commatus, C. fimetarious

Caps are 1.5-4cm wide, at firstelongated oval, later conical, thencompanulate; surface white andcovered with small white scales thatdisappear within a few hours,margin splitting as cap expands,turning into umbrella shape atdissolution. Gills 6-10cm long, upto1 mm wide, free; first white, soonturn black on liquifying stem 2-4"long, 2-3mm thick, white, shinning,hollow, fragile, tapering upwardswith a small bulb at the base. Spores

8-12x3-5mm, elliptic and black (Kaulet al., 1978).

Epidemiology

The infection generally comesthrough unpasteurized or partiallypasteurized compost or casing soil orair. Ink caps appear if the compostcontains too much N, so if too muchchicken manure is used, or if thepeak heating period is too short.These are therefore, genuineindicator moulds which arebenefited from insufficientlyconverted N containing constituentslike NH3. Ink caps can also develop

Symptoms of Ink caps

31


if insufficient gypsum is added to thecompost or if peak heating has takenplace at too low a temperature or ifthe compost is too wet and poor intexture. Ink caps can directly usefree NH4 + and can also decomposecellulose very well, in addition tolipids and lignin. They are genuinecoprophillic fungi which have anoptimum pH of around 8. The largemasses of spores released throughinking of the caps can very easilyinfect freshly prepared compost.

Control : Use properly pasteurizedcompost and casing soil. Avoidexcessive watering. Rogue out youngfruit bodies of the weed fungus toavoid its further spread.

12. CINNAMON MOULD

Pathogen : Chromelosporiumfulva, C. ollare

Common name : Cinnamon brownmould, brown mould

The occurrence of this could hasbeen reported in mushroom bedsfrom J&K (Kaul et al., 1978) Punjab(Garcha et al., 1987) and differentparts of HP (Sohi, 1988).

Symptoms : AlthoughChromelosporium fulva(Ostracoderma fulva) has been

called cinnamon brown mould, itscolour ranges from yellow gold togolden brown to cinnamon brown.The mould first appears as largecircular patches of white aerialmycelium on the compost or casing.Within few days the spores areformed and the colour changes fromwhite to light yellow or to lightgolden brown. As the spores mature,the colour changes to golden brownor cinnamon and the colony developsa granular appearance. The fungusproduces numerous cup-like fleshyfruit bodies on beds.

Causal organism :Chromlosporium fulva, C. ollare

Perfect statge : Pezizaostracoderma

Apothecium discoid, varying insize from a few mm when young to1-2cm wide when mature; cupshaped, margin wavy, often splitting,tapering to a stem like base. Stem5-9mm long. Asci cylindricalmeasuring 80-160x8-12. Ascospores8 in number, arranged in a singlerow, ellipsoid, hyaline 8-12x4-8m.Paraphyses present, hyaline.

Epidemiology : Soil, casing mixtureand damp wood are the sources ofprimary inoculum. Inoculum canblow through open doors or splash

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from floor during cleaning. Thespores of the fungus are easily air-borne. Over pasteurized compost,over-heated patches during spawnrun, high moisture content of thecompost and excess of ammoniapresent in the compost favour thedisease development.

Control : Casing soil should not bemade completely sterile by steam orformaldehyde. Newly cased bedsshould be sprayed with dithane Z-78 and maintain proper moisturecontent in casing layer.

13. LIPSTICK MOULD

Pathogen : Sporendonemapurpurescens

Common name : Lipstick, Redlipstick

This disease has been reportedfrom mushroom farms in Punjab(Garcha et al.,1987) and HP (Sohi,1986, 1988).

Symptoms : The disease firstappears in spawned compost as awhite crystalline-like mould, rather

Symptoms of lipstick mould

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nondiscernable from spawn. As thespore of the mould mature, thecolour changes from white to pink,to cherry red and then to dull orangeor buff. White mycelial growth ismore in loose areas of casing and cancolonize well conditioned compost. Incrops where there is a serious virusdisease, lipstick mould usuallyoccurs as a secondary disease.

Causal organism : Sporendonemapurpurescens

Mycelium whitish at first, oftentaking on a frosty appearance andthen forming whitish balls ofmycelium. Hyphae septate andbecome segmented into chains of l-celled, short cylindric spores withtruncate ends. Spores have reddishpigment which gives the whitishmould a cherry red colouration.

Epidemiology : Soil, casing mixtureand spent compost are the sourcesof primary inoculum. It is furtherdisseminated by water splashes orpickers. The mould is reported to beassociated with the use of chickenmanure in the compost formula; thelitter is said to carry the lipstickfungus.

Control : Good hygiene is essential.Good pasteurization andconditioning of the compost willeliminate the pathogen.

14. LILLIPUTIA MOULD

Pathogen : Lilliputia rufula (Berk& Br.) Hughes

This competitor mould has beenreported from HP and Delhi (Sethand Munjal, 1981) with an incidenceof 1-40% during 1975-1979,maximum being in Chail (HP). Itseriously restricts the spawn spreadin the compost resulting in pooryields. The sexual stage has beenidentified as Gliocladium prolificumBainer. Chicken manure, horsemanure as well as casing mixture arethe primary sources of infection.Mycelium is viable upto 3 months (at10C) and cleistothecia upto 9months under room temperature.Use of dithane Z-78 at 20ppmconcentration has beenrecommended for the control of themould. (Seth and Munjal, 1981).

15. PINK MOULD

Pathogen : Cephalotheciumroseum Corda

This mould has been observed inJ&K (Kaul et al., 1970) and Chailand Solan in HP as a white growthon the casing soil which turns pinkin due course (Seth, 1977; Sohi,1986). Yield loss upto 90% or evencomplete crop failures have also

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been recorded. Hyphae are septateand branched. Conidiophores erect,usually branched and slightlyswollen at the tip. Conidiaacrogenous, single, pear shaped, 2-celled, the apical cell being larger,hyaline to pink, 11-18x7.5-9.5m.Infection generally comes throughair. Mould can be checked byspraying twice thiram or captan(0.04%) on casing soil at 10 dayintervals (Guleria and Seth, 1977).

16. OEDOCEPHALUM MOULD

Pathogen : Oedocephalumfimetarium, Oedocephalum spp.

This is a common mouldobserved on mushroom beds in HPand incidence upto 60% has beenobserved in a farm at Solan during1991 (Sharma, 1991). Artificialinoculation of casing layer with O.fimetarium @ 5g inoculum per 10kgcompost bag has reduced thenumber and weight of fruitingbodies by 19.9% and 11.63%,respectively (Sharma, 1991; Sharmaand Vijay, 1993). The mould formsirregular, light silver gray patches onthe compost surface during cooldown before spawning. Afterspawning, the mould is light gray butchanges to dark tan or light brownas the spore mature. Similar growthis also recorded on casing layer.

Conidiophores of the fungus areerect with a spherical cluster of largespores at its tip end. Oedocephalumsp. in compost indicates thatammonia and amines were notcompletely eliminated duringpasteurization and conditioning.Spraying or swabbing locally with 2%formalin controls the mould.

17. WHITE PLASTER MOULD

Pathogen : Scopulariopsis fimicola

This disease has been reported tooccur commonly in different parts ofIndia by several workers (Garcha,1978; Kaul et al. 1978; Sohi, 1986;Bhardwaj et al. 1989) causing about37% loss in yield. The diseaseappears as white patches on thecompost or casing soil. Thesepatches or mycelial mats may bemore than 50cm under favourableconditions. The white growthchanges to light pink after a week ofthe formation of the spot. Spawn runis reduced significantly and undersevere conditions complete cropfailure are also recorded. Myceliumof the pathogen is septate,conidiophore short, branched, borneirregularly as lateral branches ofhyphae. Annellospores ovate,globose, round or showingtruncation, buff to avellaneous inmass, occur in chains or clusters,

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measure 4.8-9 x 4.8 m. Thepathogen is favoured by under orovercomposted compost which stillretains the smell of ammonia andhas high pH (more than 8). Propercomposting and addition of optimumquantities of water and gypsum arerecommended. Sprays of benomyl(0.1%) and local application offormalin (4%) after the removal of themat are helpful in controlling thedisease.

B. OYSTER MUSHROOM(Pleurotus spp.)

a. Diseases

There are four fungal diseasesreported on oyster mushroom fromIndia. Their causal agents,symptoms and control measures arepresented in Table 1.

b. Competitor moulds/weedmoulds

Compared to white buttonmushroom, the information ondiseases and competitor mouldsoccurring in or on oyster mushroomsis less. Several competitor mouldshave been reported occurring in thesubstrate used for oyster mushroomcultivation. Variations in thenumber and types of moulds aremainly due to the use of a variety of

substrates, different methods ofsubstrate preparation and theconditions and containers used forcultivation.

Competitor moulds: Differentfungi occurring in the substrate andcompeting with mushroommycelium for space and nutritionare: Arthrobotrys sp., Aspergillusniger, A.flavus, A.fumigatus,Alternaria alternata,Cephalosporium aspermum,C.acremonium, Chaetomiumglobosum, Cladosporiumcladosporoides, Coprinus retirugis,C.sterguilinus, Coprinus spp.,Cochliobolus specifer, Drechslerabicolor, Furarium moniliforme,f.moniliforme var. ferbolutinans,F.moniliforme var. subglutinans,F.graminearum, Momniellaechinata, Mucor sp., Penicillium sp.,Rhizopus oryzae, Rhizopus spp.,R.stolonifer, Stachybotryschartarum, Stilbum nanum,Stysanus medius, Sclerotium rolfsii,Sordaria fimicola, Oedocephalumgloberulosum, O.lineatum,Trichoderma viride, Trichotheciumroseum, Trichurus terrophilus andPhialospora sp. (Sharma andJandaik, 1980, 1981; Singh andSaxena, 1987; Doshi and Singh,1985; Vijay and Sohi, 1989; Das andSuharban 1991). Loss in yield in

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Table-1: Fungal diseases of oyster mushrooms in India

SN Casual organism Symptoms Control References

1. Cladobotrym apiculatum White cottony growth Spray bavistin Upadhyay etC.verticillatum on the substrate; small 50ppm al; 1987;SohiC.variospermum brown irregular sunken and

spots or fluffy growth on Upadhyayfruit bodies; soft rot and 1980;decay of sporophores Goltapeh etemitting foul smell. al. 1989

2. Gliocladium virens Fruit bodies covered by Spray 100ppm BhardwajG.deliguescens mycelium and green bavistin or et al. 1987;

spots; young pin-heads benomyl Sharma andbecome soft, brown, pale Jandaik,yellow and decay. 1983Mature fruit bodies showbrown spots enclosed byyellow halo.

3. Arthrobotrys pleuroti Fluffy growth on Spray 50ppm Ganeshan,substrate and fruit bavistin 1987bodies; infected tissuesturn yellow, waterlogged and rot.

4. Sibirina fungicola Powdery white growth Proper Sharma andon stipe, gills and the aeration and Jandaik,primordia; primordia RH essential; 1983,show brownish spray benomyl Jandaik anddiscolouration and soft twice Sharma,rot and mature fruit 1983.bodies turn fragile.

different Pleurotus spp. by thesecompetitor moulds has beenreported upto 70%. In addition tothese moulds being competitivesome have been shown to producemetabolites which directly inhibitthe growth of mushroom mycelium.However, detailed information about

these competitor moulds especiallyon their relative importance,epidemiology and management isnot yet available. Most of thecompetitor moulds have beenreported to be completely inhibitedunder in vitro and/or in vivoconditions by benomyl (50 ppm),

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carbendazim + blitox (100ppm each)and Thiram (100ppm) (Bano et al.,1975, Doshi and Singh, 1985;Sharma and Jandaik, 1980).

C. PADDY STRAW (Volvariellaspp.)

Though paddy straw mushroom(Volvariella spp.) was the first to becultivated in India as early as 1943by Thomas and his associates atCoimbatore yet very littleinformation is available on thediseases of this mushroom. This isstill being cultivated outdoors inIndia following primitive productiontechnology with very low biologicalefficiency. Paddy straw mushroomsare subject to a number of destructivediseases/competitor moulds likeMycogone perniciosa, Scopulariopsisfimicola and Verticillium spp. inother countries. In India, largenumber of competitor moulds andfew diseases have been reported onthis mushroom. Chaetomium spp.,Alternaria sp. and Sordaria sp. havebeen commonly observed ascontaminants on wheat, kans, maize,barely and jowar beds but not onlypaddy straw bundles (Gupta et al.1970). A button-rot disease causedby Sclerotium sp. has been reportedby Muthukrishnan (1971) andbacterial button-rot by Kannaiyan

(1974). Combination of insecticide,fungicide and antibiotic (Malathion0.025% + dithane Z-78 or benomyl0.025% + tetracycline 0.025%) arerecommended for the managementof pests and diseases (Kannaiyanand Prasad, 1978). Several othercompetitor moulds namely, Coprinusaratus, C.cinereus, C.lacopus,Psathyrella sp., Penicillium spp.,Aspergillus spp., Rhizopus sp.,R.nigricans and Sclerotium spp.have been reported from thesubstrate (Munjal, 1975; Bahl, 1984;Purkayastha and Das, 1991,Rangaswami, 1978). Partialsterilization of the straw and sprayson the beds with captan and zineb(0.2%) have been recommended forreducing the damage. Bahl andChowdhry (1980) have reportedPodospora favrelii as a seriouscompetitor and inhibits the growthof mushroom mycelium completely.Bhavani Devi and Nair(1986) havealso recorded Rhizoctoria solani onthe substrate which reduces thesporophore formation and causesmalformation of fruiting primordia.A serious effort is urgently neededto investigate the diseases of paddystraw mushroom and recommendthe package of practices to befollowed to the growers to achievegood yields.

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D. OTHER MUSHROOMS

Sporadic attempts have beenmade to cultivate few othermushrooms like giant mushroom(Stropharia rugoso-annulata), blackear mushroom (Auriculariapolytricha), shiitake (Lentinulaedodes) and milky mushroom(Calocybe indica) in different partsof the country and the competitormoulds/diseases recorded on themare briefly mentioned below:

Sohi and Upadhyay (1989) havereported Mycogone roseaparasitizing S.rugoso-annulataunder natural conditions. The mainsymptoms are white cottony growthon gills, light brown spots on stipeand deformity of the sporophores.Cladobotryum verticillatum hasbeen reported on Auriculariapolytricha (Goltapeh et al. 1989)producing white fluffy growth onsubstrate and fruit bodies resultingin 9-96% yield loss. Sprayingcarbendazim (50ppm) has beenreported effective for controlling thedisease. Trichoderma viride,Trichoderma sp., Aspergillus spp.and Fusarium sp. have beencommonly recorded as competitors(Sharma and Thakur, unpublished)during the cultivation of winter earmushroom. During the cultivation ofC.indica, several competitor moulds

namely, Aspergillus niger, A.flavus,A.fumigatus, Rhizopus stolonifer,Mucor sp., S.rolfsii, T.viride,T.haematum, Fusarium spp. andCoprinus spp. have been isolatedfrom the substrate (Doshi et al.1991). In addition Sharma andThakur (unpublished) have alsorecorded very high incidence ofCladobotryum and Oedocephalumspp. from the casing mixture.Incidence of T.viride has beenrecorded from 15-25% in thesupplemented bags as compared to5-10% in unsupplemented ones inL.edodes cultivation (Thakur andSharma, 1992).

GENERAL GUIDELINES

In order to decide the mosteffective measures for controlling adisease in mushroom, it is necessaryto understand the size of the initialinoculum, density, the rate at whichthe disease develops and spreads andthe time when the infection takesplace.

Based on these, the followingpreventive and/or eradicative controlmeasures are necessary for themanagement of these diseases:

Ecological-by manipulations ofenvironmental factors such astemperature, humidity andventilation.

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Biological-by use ofantagonistic organisms throughincorporation of biocontrolagents and organic amendments.

Chemical-by use of safe andminimum doses of specificfungicides, antibiotic etc.

A close relationship existsbetween crop management practicesand some endemic disease problemslike dry bubble, brown blotch andtruffle. Biological agents are beingincreasingly tried throughout theworld but with a limited applicationon commercial scale. Sanitation andhygienic measures are mostessential to manage the diseaseparticularly under Indian conditionsalthough under certain situationsuse of chemicals is also inevitable.

Sanitation and hygiene

Hygiene covers all the measureswhich are necessary to allow as littlechance as possible to the pests andpathogens to survive, develop andspread. Thus hygiene and sanitationgo hand in hand at all stages ofgrowing mushrooms. Farm hygieneis the best defense a mushroomgrower has against mushroom pestsand diseases particularly during thepresent days, when use of chemicalson food crop is being discouraged.

After having gone through thedetails of different diseasesdiscussed earlier we know thatmushroom pathogens gain entry toa mushroom farm in a variety ofways. They can fly in, drift in on thewind and crawl in. Also they can becarried on people, on the vehiclesand in the raw materials. Whatmakes matter worse is that they areusually difficult or impossible to beseen with the naked eyes. Based onthe critical observations during allthe stages of mushroom production,the following steps have become aroutine practice for successfullycultivating mushroom.

The location of mushroom unitshould be in such an area whereeffluents of chemical industriesdo not pollute the water and alsothe air is free from toxic fumes orgases.

Floor for the preparation ofcompost should be cemented/tiled and covered with a roof.

Substrates used for compostpreparation should be fresh,protected from rain and mixed inexact proportion.

Pasteurization and conditioningof the compost should be foroptimum duration at right

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temperatures as over/underpasteurization may not producequality compost and invite manydisease problems.

Do not allow free access ofpersons working in compostingyards to spawning and othercleaner areas without changingthe dress and foot-dip. Similarly,all machinery including tractorsand fork-lift trucks should not bemoved to the cleaner areas. Afterfilling, all equipment andmachinery should be thoroughlycleaned.

Spawn should be fresh and freefrom all the contaminants.

All equipments used forspawning, floor and walls ofspawning area must be washedand disinfected.

The fresh air should be filteredbefore it enters the growingrooms to exclude all particles of2 micron and above.

Casing mixture should beproperly pasteurized (60-65C for5-6 hours).

Casing mixture should be storedin a clean and disinfected place.

All the containers, equipmentsand machinery used for casingshould be thoroughly washedand disinfected. Keeping dust toa minimum and not to have dustyoperations going on at the sametime elsewhere on the farm isalso very helpful.

The pickers should use cleanoveralls and gloves. Pickingshould start from new or cleanercrop towards older crops.

Waste from picking, chogs, trash,stems, unsaleable mushroomsshould be carefully collected notallowing to fall on the floor, andbe disposed off carefully.

Avoid surface condensation ofwater on developing mushrooms.

Add bleaching powder (150ppm)at every watering to managebacterial disease.

Remove heavily infected bagsfrom the cropping rooms or treatthe patches by spot application of2% formalin or 0.05% Bavistin.

Maintain optimumenvironmental conditions in thecropping rooms to avoid abioticdisorders.

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Control insect-pests well in timeto avoid the spread of pathogenby them.

At the end of crop, cooking out at70C for 12 hours is very essentialto eliminate all pests andpathogens.

Use of Chemicals

It is advisable to manage thedisease in mushrooms throughhygienic measures listed above.There are only a limited number ofpesticides registered for use onmushrooms. This is becausemushrooms themselves are fungiand most of the pathogens are alsofungi thereby making the choice offungicides very difficult. Moreover,because of short cropping cycle,residual toxicity of differentchemicals is of great concern and itmust be kept below the tolerancelimit. Mushrooms are very sensitiveto fumes, toxic gases and severalchemicals. This also limits thefrequent use of chemicals inmushroom industry. Equallyimportant factor which limits theuse of fungicides for themanagement of diseases inmushrooms is the problem ofresistance. Repeated and regularapplications of the same chemicalgreatly increase the chance of

resistance. If equally effectivealternate fungicides are available theproblem of pesticide resistance canbe minimized. On the other handthere are, unfortunately only a fewpests or diseases that can becontrolled satisfactorily byenvironmental manipulation alone.Some of the most common fungicidesrecommended for the control ofmajor fungal pathogens ofA.bisporus (Fletcher et al. 1986) andused in mushroom industry are:

Benomyl(Benlate 50wp)- Forcontrol of Dactylium, Mycogone,Trichoderma, Verticillium, mix240g/100m with casing ordissolve in water at 240g/200litres/100m during firstwatering.

Carbendazim (Bavistin) same asfor benomyl.

Chlorothalonil(Bravo or Repulse)- to control Mycogone andVerticillium. Apply as spray 2week after casing and repeat notless than 2 weeks later @ 200mlin 100-200litre water/100m.

Prochloroz Manganese(Sporgon)- to control Mycogone,Verticillium, Dactylium, give asingle application of 300g/100litres/100m, 7-9 days after

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casing. For double application,use 113g/100litres/100m, 7-9days after casing and repeat againbetween second and thirdflushes. For triple application,use 57g/100litres/100m, 7-9 daysafter casing and after first andthird flushes.

Thiabendazole(Tecto)- to controlDectylium, Mycogone,Verticillium, apply at the samerate as Benomyl.

Zineb(Zineb Tritoftoral)- tocontrol Dactylium, Mycogone,Red Geotrichum and Verticillum,Use 7% dust, at 350g/100mevery week after casing or 140g/100m before watering. Forwettable powder, 1kg/1000 litres@ 5 litre/100m after casing andbetween flushes. For Tritoftoral,5kg/100m at 4.5m betweenflushes.

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III. VIRAL DISEASES

including mycoviruses, fungalviruses, mycophages, doublestranded RNA (dsRNA) plasmidsand virus-like particles (VLPs). Theterm mycophage is clearlyunsuitable since virus infection hasvery rarely been associated with lysisin fungi. Although mycoviruses mayshare some of the characteristics ofplasmids, their morphology,nucleoprotein composition and thepossession of virion-associated RNApolymerase activity are consistentwith a viral nature. The termplasmid has already been abused incurrent literature as pointed out byReanney (1976) and to denote theviruses of fungi as plasmids wouldnot find ready acceptance. The termVLPs and mycoviruses have beenused by some authors (Bozarth,1972; Saksena and Lemke, 1978),with the understanding that thefirst term applies to those particlesoccurring in fungi and having avirus-like appearance in electron-micrographs but which have notbeen isolated and characterised,whereas the second term denotesthose which have been isolated andshown to have the morphology andnucleoprotein composition generally

a) Button Mushroom

INTRODUCTION

In recent years, viruses haveincreasingly been found inassociation with fungi, an associationthat has taken one of the two forms.In the first, the fungus is the vectorof the virus and in the second,fungus is the host of the virus. Hereonly the second form of associationi.e. fungi, especially the mushrooms,as hosts of viruses will be consideredin detail which has been reviewedearlier by Raychaudhury (1978),Sharma (1991) and Sharma andKumar (2000). Although thepresence of viruses in fungi has longbeen suspected (Sinden and Hauser,1950) experimental evidence wasnot forthcoming until 1962 whenvirus particles were demonstrated indiseased mushroom (Gandy andHollings, 1962; Hollings, 1962). Todate viruses or virus-like particles(VLPs) have been reported to occurin over 100 species from 73 generaof fungi, but only a small number ofthem have been isolated andcharacterised. Several terms havebeen used for the viruses of fungi

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attributed to viruses. Thisdistinction offers an operationalconvenience and has been widelyadopted. Since mycoviruses havenot conclusively proven to beinfectitious as purified particles,some workers prefer to apply theterm VLPs in all cases.

HISTORY AND GEOGRAPHICALDISTRIBUTION

In 1948 a very seriousinfectitious disease of white buttonmushroom (Agaricus bisporus(Lange) Sing.) was observed in theUnited States of America on a farmin Pennsylvania run by the LaFrance brothers, and thus becameknown as La France disease (Sindenand Hauser, 1950). In England, adisease inducing brown staining onthe stipe was named as browndisease by Storey (1958). Gandy(1958) observed the most commonsymptom in the form of large waterlogged patches on stipes ofmushroom from diseased beds andproposed the name watery stipe. Asimilar, possibly the same diseasewas observed in the mushroomindustry throughout Pennsylvania.The cause of this disease wasunknown and no existingdescription appeared to fit thedisorder, hence the name X-diseasewas coined by Kneebone and co-

workers (1961). Since 1959 asimilar disease mushroom-die-backhas been studied in Englandwherein degeneration of myceliumrather than the symptoms on fruitbodies were more predominent andhas been attributed to a complex ofatleast three

Disease Competitor Moulds Dr. S.R. Sharma

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