6 Wood Discoloration
6 Wood Discoloration
6 Wood Discoloration
Create successful ePaper yourself
Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.
8.3 Tree Rots by Macrofungi 191<br />
single cases up to 55 m; maximum age of an individual genet around 200 years<br />
(Queloz and Holdenrieder 2005);<br />
Physiology: white rot, root rot, butt rot, so-called red rot due to reddish<br />
discoloration of the wood; at initial decay preferential lignin degradation, later<br />
simultaneous white rot (Peek and Liese 1976); parasite and saprobe;<br />
Characteristics: anamorph Spiniger meineckellus (A.J. Olson) Stalp.<br />
(Fig. 8.14C) on agar and fresh wood samples at high relative humidity: clubshaped<br />
thickened conidiophore after spore dispersal like a morning star<br />
(“Brefeld conidia” as identification feature: Brefeld 1889); flask-shaped increase<br />
of the stem basis of spruce by cambial irritation; resin excretion;<br />
Fruit body (Fig. 8.14A): annual to enduring crusty brackets in autumn,<br />
often resupinate (1 cm thick, 3–20 cm wide) in rows and roofing tile-similar,<br />
usually fused, at the stem basis and on flat-running roots, frequently covered<br />
by needle litter; yearly a new pore layer; fresh: tough, old: hard and woody;<br />
upper surface: bumpy-wrinkled, brown, often zonate, leathery-crusty, whiteyellowish<br />
margin; pore surface: white-cream with circular-angular pores (4–<br />
5/mm); dimitic; bipolar.<br />
Significance: The fungus is one of the most important pathogens in coniferous<br />
forests of temperate regions (Hartig 1874, 1878; Rishbeth 1950, 1951;<br />
Zycha et al. 1976; Hallaksela 1984; Tamminen 1985; Benizry et al. 1988; Schönhar<br />
1990; <strong>Wood</strong>ward 1992a, 1992b; LaFlamme 1994; <strong>Wood</strong>ward et al. 1998;<br />
Heydeck 2000; Greig et al. 2001; Gibbs et al. 2002; Korhonen and Holdenrieder<br />
2005), which causes substantial damage particularly in older forests. The infection<br />
occurs by germinating spores or by mycelium that is already present<br />
in roots or soil. Several infection ways are possible: by basidiospores (also<br />
conidia) via stump infection (Redfern et al. 1997), by mycelial growth through<br />
root graft transmission from diseased to healthy roots (Hartig 1878; Schönhar<br />
2001), or via spores [germinable about 1 year: Brefeld (1889)], which are<br />
washed into the soil by rain and germinate on the roots. The fungus penetrates<br />
into older roots through wounds and into young uninjured roots through the<br />
thin bark (Rishbeth 1951; Peek et al. 1972a, 1972b; Lindberg and Johansson<br />
1991; Lindberg 1992; Solla et al. 2002). The hyphae penetrate into sound spruce<br />
roots via the pit channels of the thick-walled stone cork cells. The walls of the<br />
following thin-walled stone cork cells and the sponge cork cells are degraded.<br />
The fungus colonizes the tracheids from the bark rays via the wood rays. The<br />
tracheids are degraded by enzymes and perforated by microhyphae (Peek and<br />
Liese 1976). Embryos of Pinus spp. showed three days after artificial inoculation<br />
intercellular penetration of hyphae through the epidermis and into the cortex<br />
(Nsolomo and <strong>Wood</strong>ward 1997). Infection of spruce seeds of 4–7 days of age<br />
showed that infective structures on the root surfaces were evident 24 h after<br />
inoculation. Internal colonization of cortical tissues started after 24–48 h and<br />
reached the endodermis within 72 h. Severe destruction of stelar cells occurred<br />
12–15 days postinfection (Asiegbu et al. 1993). Infection of nonsuberized and<br />
www.taq.ir