UKTC Archive

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

Subject: RE: Ganoderma applanatum/australe on n.maple - implications
From: Viper Snake
Date: Dec 30 2011 09:40:43

Dear Luke,
1) Regarding point 3 below my understanding is that the statements in the 
quoted references of F. hepatica principally colonising heartwood are based 
on observations.
1) Just as my findings are based on observations of the contrary inside out 
strategy of (totally) degrading annual sapwood rings by F. hepatica.
2) However I know that in 2000 Schwarze, Balm and Fink published a paper in 
Mycological Research with the title: Dual modes of degradation by Fistulina 
hepatica in xylem cell walls of Quercus robur. I found it very interesting.

2) So did I, because that is where the first reference was made to F. 
hepatica also being capable of soft rot eleven years ago.
3) I may not be totally understanding your use of the term: 'typically shaped 
morbid growth and necrosis of living tissues and bark.' Originally I took it 
to mean wood with reduced vitality, dead areas of wood, and bark in declining 
health leading to death. Is this correct?

3) No, both Tony and I have documented the "typically shaped morbid growth 
and necrosis of living tissues" with lots of photo's, some of which you can 
find on Arbtalk.
1) Thank you for taking the time to reply although it appears to me that 
you are opening more questions than answering existing ones. 

1) Would you be so kind to answer my questions first before posing new 
questions to which you expect an answer ?

2) Have you any thoughts about competition between different species 
mycorrhizal fungi for soil volume ? For example ericoid mycorrhizae 
associated with heather competing with ecto and VA mycorrhizae associated 
with trees ? 

2) Yes, I have and they will be published in my Dutch book on the tree 
species specific ecosystem in September 2012.

3) Lonsdale (1999, p. 99), Schwarze et. al. (2000, p. 76-81) and Butin 
(1995, p. 163). Schwarze et. al. (2000)

3) Isn't this all literature based upon in vitro research of dead wood ? 
And does any of the authors explain where the acid in the fruitbodies of F. 
hepatica comes from, why F. hepatica is restricted to "white oaks" such as 
Q. robur/petrea and to C. sativa and what process or pathogen other than F. 
hepatica causes the typically shaped morbid growth and necrosis of living 
tissues and bark, that only occurs in these tree species while being 
colonised by F. hepatica ?

4) Sapwood redundancy may occur after loss of root function or crown volume 
and associated foliage. 

4) Which IME never is the case with, nor the effect of an infection of 
living tissues by the mycelium of F. hepatica.


First some general remarks and questions :

- Where does the sour vinegar taste of fruitbodies of the often guttating 
"poor man's beefsteak" F. hepatica come from, that makes it necessary to 
soak it in milk or wine overnight before it can be consumed, if not from 
the acids the sapwood of Q. robur/petrea or C. sativa secretes when living 
tissues are invaded and "tapped" by the mycelium of F. hepatica ?
- As I said before, it has been assessed, that F. hepatica "feeds on" the 
sugar rich acids produced by the sapwood, acids that are no longer present 
in dead heart wood of white oaks and sweet chestnut, and that is why 
Laetiporus sulphureus can easily invade, dry brown rot and hollow the heart 
wood of these trees.
- What other pathogen do you suggest is responsible of the typical living 
tissue and bark morbid growth and necrosis that is always associated with 
the presence of the mycelium and/or fruiting of F. hepatica inside and/or 
on the tree ?
- Even when constricted to (necrotrophic) parasitic bracket fungi, the tree 
species specific ecosystem of white oaks is far more complicated than you 
present it. Along with F. hepatica and Laetiporus sulphureus, Inonotus 
dryadeus, Phellinus robustus, Daedalea quercina and Piptoporus quercinus, 
among which competition for territory and sugars takes place, play a just 
as important role in old white oaks becoming veterans on the long run.
- F. hepatica produces an atypical brownrot of (dead) sapwood, L. 
sulphureus a dry brown rot of heart wood. Inonotus dryadeus produces a soft 
rot of living tissues and a white rot of dead wood, Piptoporus quercinus 
and Daedalea quercina a brown rot of heart wood, and Phellinus robustus a 
simultaneous white rot.

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 conclusion.

1) All continental European scientific literature lists F. hepatica either 
as a wound parasite or as a (weak) necrotrophic parasite and states that F. 
hepatica is unable to infect, colonise and fruit from completely dead 
laying down or standing up wood of Q. robur/petrea or Castanea sativa, if 
the mycelium has not occupied a foothold in the tree while the tree was 
still alive, which - according to my understanding - is correct. 

2) 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 

2) My understanding is based on my concept of (the dynamics of) the tree 
species specific ecosystem with its tree species specific life cycle, tree 
species specific soil food web and tree species specific parasitic, 
saprotrophic and (ecto)mycorrhizal (macro)fungi, which are for the greater 
part responsible for the uptake of water and nutrients and for protection 
of the tree roots and the tree as a whole against drought, toxics and 
attacks from (soil) parasites with self-produced antibiotics and fungicides.

3) 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.

3) What role do (tree species specific) ectomycorrhizal macrofungi play in 
your example, how do they affect this process and how does this process 
affect the ectomycorrhizal symbionts ?

4) There are numerous ash pollards.

4) Being associated with endomycorrhizal microfungi, ash has a completely 
different tree species specific ecosystem and life cycle than tree species 
associated with ectomycorrhizal macrofungi - such as oaks and beech - have.

5) 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.

5) Did your friend also study the role (ecto)mycorrhizal (macro)fungi play 
in the soil food web and the influence they have on the development or 
inhibition of soil pathogens ?

6) 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.

6) See 1).

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

7) I already said, that other than white oaks such as Q. robur/petrea and 
Castanea sativa, red oaks, such as Q. rubra, lack the acids in their living 
tissues the mycelium of F. hepatica needs to "feed on".

Best wishes for 2012,

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