Pine wilt is caused by the nematode Bursaphelenchus xylophilus and is one of the most serious tree diseases in Japan. From the end of 1980s, many oak forests on Honshu Island have been damaged by Raffaelea quercivora. In additon, Ceratocystis spp. are killing spruce and larch trees in northern Japan. All the pathogens of these diseases are vectored by beetles. The leaves of pine trees become discolored about three weeks after inoculation with the pine wood nematode (Kuroda et al. 1988). Usually, healthy trees do not wilt very easily, even when the supply of water is stopped for a certain period. Why these pathogens can kill trees so effectively is a question that remains to be answered. Furthermore, the cause of the swift death of the apical and cambial cells of a huge tree does not yet have a theoretical explanation.
In healthy trees, xylem sap ascends spirally in pine trunks. In trees infected with pine wilt, dehydration occure in the sapwood and gas-filled areas emerge in the trunks prior to leaf discoloration (Kuroda et al. 1988). Such dysfunctional areas enlarge, and the tree wilts within one or two months for the water deficit. It is clear that some kind of a system rapidly excludes the xylem sap from the tracheids (Kuroda 1989, 1991). In the case of oak trees infected with Raffaelea quercivora., the discoloration of sapwood and blockage of water are well underway before the appearance of other symptoms of wilt in the summer months (Kuroda 2001, Kuroda and Yamada 1996, Takahata and Ikeda 2001).
The mechanism of the symptom development of wilt described here (Fig. 1) is based on research into the pine wilt and oak mortality caused by Raffaelea quercivora. When microorganisms attack a tree, a protection strategy is set in motion. A synthesis of secondary metabolites starts in the tree tissue. With this reaction, cavitation or discoloration occurs in the xylem. Tracheids and vessels become dysfunctional and are filled with air. Unfortunately, the secondary metabolites are ineffective in their efforts to protect the tree against the pine wood nematode and Raffaelea sp. As the pathogen is widely distributed, protection occurs in many places in a tree, and, therefore, xylem dysfunction is widely spread. The sap ascent is extensively reduced, and the tree dies because of a water deficit. I considered that these findings might be applicable to other wilt diseases. To check this possibility, wilt processes in larch and spruce trees were monitored after inoculation with the pathogens Ceratocystis lalicicola and C. polonica, respectively. Investigations were made with techniques involving Acoustic Emission (AE) to detect embolism and cavitation in tree trunks (Kuroda 1995, Kuroda and Kuroda 2000), a dye injected into tree trunks to trace the course of sap ascent, and anatomical analyses to check cytological reactions of host cells and hyphal distribution.