UKTC Archive

RE: Ganoderma applanatum/australe on n.maple - implications

Subject: RE: Ganoderma applanatum/australe on n.maple - implications
From: luke steer
Date: Dec 27 2011 20:06:53
Dear Gerrit,

I’ve written my answer to your question after selected text from our earlier 
emails to provide context. 

 

Gerrit 1

"4. Of which Fistulina hepatica is an example, as it first "feeds" on tannin 
or vinegar acids produced by the sapwood of the tree (Quercus robur/petrea, 
Castanea sativa) in defense, without causing a problem to the stability of 
the tree, because after the mycelium finally enters the cambium and causes a 
necrosis of living tissues and bark from which exposed (dead) sapwood it 
fruits, the tree compensates for the loss of stability in a tree species 
specific way (see : 
http://arbtalk.co.uk/forum/members/fungus-albums-fistulina-hepatica.html ), 
which is a good example of co-evolution between fungus and tree species."

 

 

Luke 1

The paragraph quoted above appears to indicate that you consider that 
Fistulina hepatica can kill sapwood and cambium. I'm afraid that this is 
quite different from my understanding that F. Hepatica is purely a saprotroph 
that is specialised to colonise and gain its nutrition from heartwood. 
However, I'll accept that it may also be able to obtain nutrition from dead 
sapwood if not 'out-competed' by wood decay fungi that are more able to 
utilise this substrate. I'm sure that we are all aware that sapwood and 
cambium may die for a multitude of reasons: biotic, abiotic, but most often a 
combination of a number. My understanding was that, once dead, F. hepatica 
maybe able to utilise the newly available substrate as a secondary 
saprotroph. If it's not too much trouble could you please recount the steps 
you've taken to eliminate these potentially primary reasons for sapwood and 
cambium death and enabled you to come to your conclusions. 

 

Gerrit 2

Instead of answering, a question in reply : how do you account for the morbid 
growth and necrosis of living tissues and bark appearing once the mycelium 
has entered the cambium, a phenomenon I have documented on living "white" 
oaks (Quercus robur/petrea) and sweet chestnuts hundreds of times, if F. 
hepatica is not parasitic ?

And why is the (sap wood of the) "red" oak Quercus rubra never affected by 
Fistulina hepatica ?

 

Regards,

Gerrit                                

 

Luke 2

Gerrit, below I give some background information for my current understanding 
before I provide my answer based on that.

 

My understanding is based on trees being balanced, as are all plants.  If 
something occurs to one part of the plant ramifications occur throughout it.  
For instance, if we experience drought, tree roots won’t be able to supply 
sufficient water and nutrients, leaves wilt and potentially die.  When this 
occurs, and the foliage area of the tree is significantly reduced, some roots 
and sapwood will also become physiologically dysfunctional.  

 

Another example is when foliage is removed, potentially by storm damage or 
chainsaw.  With a reduced amount of foliage the tree has reduced requirements 
for water and nutrients so some of its roots and sapwood become redundant and 
eventually physiologically dysfunctional.  The same can be said if roots are 
removed by either trenching or root diseases: the remaining roots won’t be 
able to supply the requirements of the amount of foliage present prior to the 
root death event so some of that, along with some sapwood, will die and 
become available for colonisation by saprotrophic decay fungi. 

 

Some buffering can occur but I imagine that this depends on the tree’s energy 
reserves.  

 

When sapwood dies it usually dies from the inside out and the live cylinder 
of physiologically functional sapwood becomes thinner.  We see this with 
pollarded trees: healthy lapsed pollards grow large crowns and create and 
maintain a relatively thick live cylinder of sapwood.  If a tree is pollarded 
regularly it doesn’t have the opportunity to form a large crown, its trunk 
hollows and it is only able to maintain a relatively thin cylinder of 
physiologically functional sapwood.  There are numerous ash pollards in the 
Lake District that illustrate this.  However, occasionally, and especially 
with trees with large trunk diameters, they can lose so much foliage that 
they are not able to maintain a complete cylinder of physiologically 
functional sapwood and strips of dead bark and sapwood form on the trunk.  
There are numerous examples of this in Sherwood Forest Country Park – few of 
the trees have full crowns and many observers consider that there has been a 
massive crown reduction event that affected the majority of the trees at some 
time in the past.  

 

I’m sure that you probably know better than most that soil is chocka-block 
with organisms including some that feed on live roots such as native species 
and strains of Pythium and Phytopthora.  I have a friend who did his PhD. On 
these at Aberdeen University.  Under normal conditions the tree can tolerate 
their presence but, if conditions alter and become ‘stressful’ for the tree 
or beneficial for an organism that is normally only a weak pathogen, it may 
kill a significant amount of tree roots.  If this were to occur the tree may 
appear drought stressed, its foliage cover reduce and portions of its sapwood 
may become dysfunctional and available for colonisation by saprotrophic wood 
decay fungi.  

 

I’m sure you are already aware of all this as it is basic ‘tree science’ so 
please forgive me if I appear patronising.  Anyway, back to your first 
question:

 

“how do you account for the morbid growth and necrosis of living tissues and 
bark appearing once the mycelium has entered the cambium, a phenomenon I have 
documented on living "white" oaks (Quercus robur/petrea) and sweet chestnuts 
hundreds of times, if F. hepatica is not parasitic ?”

 

I’ve previously considered that the ‘morbid growth and necrosis of Living 
tissues and bark’ were caused by stresses to the tree – biotic, abiotic, or 
more likely a combination of a number of stressing agents – and F. hepatica 
colonised those tissues once they became unviable.  If this is correct F. 
hepatica is a saprotrophic species.

 

I’m afraid I don’t know the answer to your second question but I would love 
to hear yours.

 

Anyway, if you have time, back to my earlier question:

“If it's not too much trouble could you please recount the steps you've taken 
to eliminate these potentially primary reasons for sapwood and cambium death 
and enabled you to come to your conclusions [that F. hepatica can act as a 
primary pathogen]?” 

 

Thank you for prompting and maintaining this stimulating discussion.

 

Regards

 

Luke

    

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 




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