Mushrooms Are Worldwide Cultivated and Consumed

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Mushrooms are worldwide cultivated and consumed.

In 2013, the global edible mushroom industry


size was valued at 34 B € [

The cultivation of edible mushrooms is susceptible to suffer certain diseases


caused by a number of diseases and pests. Fungal, bacterial and mushroom
flies conduct to significant reductions of productivity and a substantial
impact on mushroom quality. 
Mycoparasites  an organism with the ability to parasitize fungi.

Types of mycoparasitic organisms[edit]


Myco-heterotrophy[edit]
Various plants may be considered mycoparasites, in that they parasitize and acquire most of
their nutrition from fungi during a part or all of their life cycle.
Myco-heterotrophy is a symbiotic relationship between certain kinds of plants and fungi, in which the plant
gets all or part of its food from parasitism upon fungi rather than from photosynthesis. A myco-
heterotroph is the parasitic plant partner in this relationship. Myco-heterotrophy is considered a kind
of cheating relationship and myco-heterotrophs are sometimes informally referred to as "mycorrhizal
cheaters". This relationship is sometimes referred to as mycotrophy, though this term is also used for
plants that engage in mutualistic mycorrhizal relationships.

Mycoparasitic bacteria[edit]
Some bacteria live on or within fungal cells as parasites or symbionts.

Mycoparasitic viruses[edit]
Some viruses, called mycoviruses live on or within fungal cells as parasites or symbionts.

Mycoparasitic fungi[edit]
Many mycoparasites are fungi, though not all fungicolous fungi are parasites (some
are commensals or saprobes.[2]) Biotrophic mycoparasites acquire nutrients from living host cells.
Necrotrophic mycoparasites rely on dead host cells, which they might first kill with toxins or
enzymes (saprophytic growth).[2][3]

Kinds of mycoparasitic interactions[edit]


Biotrophic and necrotrophic mycoparasites[edit]
Biotrophic mycoparasites get nutrients from living host cells and growth of these parasites is
greatly influenced by the metabolism of the host.[4] Biotrophic mycoparasites tend to show high
host specificity, and often form specialized infection structures.[5] Necrotrophic mycoparasites can
be aggressively antagonistic, invading the host fungus and killing, then digesting components of
its cells. Necrotrophic parasites tend to have low host specificity, and are relatively unspecialized
in their mechanism of parasitism.[5]

Balanced and destructive mycoparasites[edit]


Balanced mycoparasites have little or no destructive effect on the host, whereas destructive
mycoparasites have the opposite effect.[6] Biotrophic mycoparasites are generally considered to
be balanced mycoparasites; necrotrophic mycoparasites use toxins or enzymes to kill host cells,
therefore necrotrophic mycoparasites are usually considered to be destructive mycoparasites.
However, in some combinations, the parasite may live during its early development as a
biotroph, then kill its host and act more like destructive mycoparasites in late stages of
parasitization.[4][6]

Mechanisms of Mycoparasitism[edit]
The four main steps of mycoparasitism include target location; recognition; contact and
penetration; and nutrient acquisition. [7]

Target location[edit]
Many research indicate that hyphal growth direction, spore germination, and bud tube elongation
of mycoparasitic fungi may exhibit tropism in response to detection of a potential host.[8] This
tropic recognition reaction is thought to arise from detection of signature chemicals of the host;
the direction of the concentration gradient determines the growth direction of the parasite. [9] As
the mycoparasitic interaction is host-specific and not merely a contact response, it is likely that
signals from the host fungus are recognized by mycoparasites such as Trichoderma and provoke
transcription of mycoparasitism-related genes.[10][11]

Recognition[edit]
When mycoparasites contact their fungal host, they will recognize each other. This recognition
between mycoparasites and their host fungi may be related to the agglutinin on the cell surface
of the mycohost. Carbohydrate residues on the cell wall of mycoparasites might bind to lectins on
the surface of the host fungi to achieve mutual recognition. [12]

Contact and penetration[edit]


Once a mycoparasitic fungus and its host recognize each other, both may exhibit changes in
external form and internal structure.[13][14] Different mycoparasitic fungi form different structures
when interacting with their hosts. For example, the hyphae of some mycoparasitic fungi form
specialized contact cells resembling haustoria on the hyphae of their hosts; others may coil
around the hyphae of their host fungus or penetrate then grow inside host hyphae. [15] Nectrophic
mycoparasites may kill host hyphae with toxins or enzymes before invading them. [3]

Brown blotch disease is a bacterial infection that affects nearly every species of
mushroom. The infecting bacteria, Pseudomonas tolaasii, produces the toxin tolaasin that
causes brown spots to cover the surface of the mushroom. Brown blotch disease is especially
problematic on common mushroom farms, where it can spread quickly and cause huge
economic losses.

Agaricus bisporus, or the cultivated mushroom, is the primary victim of brown blotch disease.
[1]
 The most common symptom of brown blotch disease in A. bisporus is the formation of round
lesions on the cap and stalk of the mushroom. [2] As the disease progresses, these lesions go
from a pale yellow to a dark brown and cause the quick deterioration of mushrooms after harvest.
[1][3]
 Any external growth such as the fruit bodies (spore-producing structures) formed by infected
mushrooms are completely brown. In minor cases of brown blotch disease, there are a few
brown spots on the cap or stalk of the mushroom. In major cases, many spots blend together and
turn all of the surfaces brown.[2]

Brown blotch disease is caused by the colonization of Pseudomonas tolaasii bacteria on the
surface of a mushroom.[1] P. tolaasii favors moist conditions, such as within water droplets or a
high relative humidity.[3] However, P. tolaasii is able to survive in a variety of environmental
conditions and successfully compete with other bacterium populations due to several biological
mechanisms, such as its ability to switch between a smooth and rough phenotypic strain.[1] In
optimal conditions, the P. tolaasii population undergoes exponential growth and also increases
the production of the toxin tolaasin.[2]
Tolaasin disrupts the plasma membranes of mushroom cells, causing their subsequent collapse.
Tolaasin does not only affect the surface of the mushroom. When secreted, it can also infiltrate
deeper hypha tissues within the mushroom.[2] Tolaasin is also an effective biosurfactant, which
means that its presence decreases the surface tension of water. Lower surface tension causes
water to spread over a larger area, enabling P. tolaasii to colonize fresh areas of the mushroom
cap.[4]
The process of infection is as follows: P. tolaasii is splashed onto the surface of a mushroom,
senses the mushroom's surface, migrates towards it, and releases tolaasin in order to
compromise the plasma membrane of the mushroom cells and access the nutrients within. [2]
Brown blotch disease spreads quickly on mushroom farms due to the close proximity of
mushrooms and favorable conditions caused by regular irrigation.

Identification[edit]
P. tolaasii presence in soil is unfavorable to mushroom farmers, so a test was created to detect
its presence. This is called the “white line test." The unknown bacteria is placed in a line on one
side of a dish and P. reactans is placed a few millimeters parallel to it. The dish is incubated at
25 °C for 48 hours. If at the end of the 48 hours there is a line of white precipitate between the
two bacterium populations, then the unknown bacterium is P. tolaasii. The line of white
precipitate forms due to a reaction between tolaasin and a compound produced by P. reactans
known as the white line-inducing principle (WLIP). The white line test can help detect P. tolaasii
in soil and prevent its spread on mushroom farms.
To prevent the spread of brown blotch disease on mushroom farms, various disinfectants and
antibiotics have been used, but none are fully effective and nontoxic to humans. [2] Chlorinated
compounds such as sodium hypochlorite are also used, but in moist conditions the growth rate of
P. tolaasii populations neutralize the effects of the compounds. [3] Therefore, the solution to brown
blotch disease is thought to be biological.
Bacteriophages have been used, but strains of P. tolaasii that are immune to such viruses have
already been identified.[2]
Introducing an antagonistic bacterium such as P. reactans, which forms the white line-inducing
principle that neutralizes tolaasin, was also seen as a possible solution. However, WLIP only
proved effective at high concentrations. [1][2]
Brown mushrooms are naturally more resistant to the brown blotch disease than their white
counterparts, so genetically engineering a more resistant A.bisporus is being researched. The
exact gene that enables this resistance has not yet been identified. [2]
One final possible biological solution is to introduce a strain of P. tolaasii without the tolaasin-
producing gene to act as a competitor. This method has not been tested. [2]
Research indicates that the incubation of harvested mushrooms at low temperatures for four
days inhibited the browning symptom, but this method has not yet been tested at a large scale. [1]

These include many orchid seedlings, as well as some plants that lack chlorophyll such
as Monotropa uniflora.
Viral Disease Top

 Virus (several)
 Double-stranded RNA
 Reduced cropping,
 bare patches on the beds,
 long-bent stalks with small caps,
 Premature opening of mushrooms,
 Stalks tapering towards the base of stalk,
 Dying pinheads
 Infected mycelium grows slowly in the beds and fruiting bodies are not produced.
 Infection of the crop at spawning lead to a higher level of disease

Spread and source of infection of virus

 Infected mushroom spores


 Mycelium from previous crops also survive in the trays
 Mushroom sheds can also release infected spores
 Dust from around the farm may introduce infected spores
 Only 10 infected spores are required for a disease outbreak.
 Farm hygiene
 Maintain 60oC temperature throughout the compost
 Filter air and seal rooms properly to prevent spores from entering during cool down phase of
compost.
 Clean equipments
 Ensure workers have clean-spare clothes
 Ensure absolute filters are fitted to spawn-run buildings

 Clean trays to prevent infection from old-infected mycelia

Green moulds

 Trichoderma koningii
 T.viride
 T.aggressivum f.sp.aggressivum
 Dark green mould patches on casing spreading to lesions on stems.

Control of green mould

 Sanitation and hygiene programme, especially targeting post crop


 Cover spots with sodium hypochlorite solution, salt, lime or gypsum and lime mix.
 Good insect and mite control
 Personnel movement patterns further reduce the spread of the disease.
 chlorothalonil at casing or mix into casing material 254 mL formulation per 100 m2 of
production
 Chlorothalonil is not effective against an established infection but lowering the infection

Cinnamon Mould

 Chromelosporium fulva (Peziza ostrachoderma)


 The color of this mold ranges from yellow gold to golden brown to cinnamon brown.
 It grows rapidly in circular patches.
 It is very common in soil, and flourishes on damp wood.
 Areas in compost overheated during spawn run may be colonized.
 Improperly conditioned compost will also support growth,
 It often occurs on sterilized soil.
 Sexual fruiting bodies may appear several weeks after the first appearance of the mold.
 Spores are airborne

1.Fungal Diseases

Dry Bubble

 Verticillium fungicola

 Muddy brown, often sunken spots on the cap of the mushrooms

 Greyishwhite moldy growth seen on pileus

 Later stage mushroom becomes dry and leathery

 Initially infected one are not develop or remain small

 Main source of infection

 Debris

 Dust on floors of growing house

 Spread

 Water splashes on healthy mushroom

 Sciarid and phorid flies over long distance

 Favorable temperature 28o c


 Poor ventilation

 High humidity

 Management of Dry Bubble

 Pick and destroy infected mushroom to prevent spread

 Sanitary conditions in growth house

 Lower the temperature to 14oc when disease noticed

 Use clean equipment

 Control flies and mites

 Bubble can destroy with salt

Management by using salt   

 Use of clean pasteurized casing media

 Properly maintained air filtering system.

 Water early infection centers with formaldehyde

 For protective measure use zineb

 Apply chlorothalonil at casing or mix into casing material

Dry bubble in Oyster

                                                    

False Truffle

 Diehliomyces microsporus

 Competitor than a pathogen

 Appears as cottony weft of mycelium on bed surface

 Wefts turn to dense small reddish brown,wrinkled,stromatic bodies resemble  a truffle

 Infected bed have peculiar disagreeable odour


 Reduced yield at mycelia exist

 Introduced through soil

Management

 Good sanitation

 Proper Pasteurization of casing material

 Low temperature during spawn run

Wet Bubble
Mycogone perniciosa

 Malformed mushrooms with swollen stipes

 Reduced or deformed caps

 Undifferentiated tissue becomes necrotic and a wet, soft rot emit bad odor

 An amber liquid appears on infected mushrooms.

 Mushrooms become brown in color

 Bubbles may be as large as a grapefruit.

 The fungus is spread via airborne dust and contaminated casing.

 It is also a parasite of wild mushrooms.

 It produces two spore types,

 one which is small and water-dispersed like Verticillium,

 second which is a large resting spore capable of persisting for a long time in the environment

Control

 Sanitation in growth house

 Clean environment around cultivation area                                                                

 Incorporating benzimidazoles in the casing.

 Benomyl at the rate of 0.95 g/m2,

 Carbendazim and thiabendazole at the rate of 0.62 g/m2

Throughout the world Sciarid flies, phorid flies, cecids, springtails, mites and
nematodes are important pests of cultivated mushrooms. These pests damage the crop
right from spawning to harvesting of the crop. Mushroom flies damage the crop directly and
also help in spreading various mushroom diseases.

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