Close-up on some aspects of fungal wilt diseases (available at www.wilt-ism.net and on DVD) Focus sur certains aspects des flétrissements causés par les champignons (disponible sur www.wilt-ism.net et en DVD)

This Web site presents a collection of articles related to fungal wilt diseases and their pathogen, with emphasis on Dutch elm disease (DED). Numerous electron microscopy (EM) micrographs are shown in the longest papers, and they generally are presented in large enough dimensions and magnifications so that readers can easily see the features at stake and follow their descriptions. The following presentation summarizes the rationale which, with time, led to the creation of this Web site. In 1954, when the senior author undertook studies on DED, which is caused by the pathogen now known as Ophiostoma novo-ulmi Brasier, a first objective was to detect pathogen occurrence in the tree and to discover its exact mode of action. Indeed, up to that point, reports of histopathological studies were based on light microscope investigations and they all mentioned that pathogen cells were rarely observed in invaded tissue. One of the explanations given to account for this phenomenon was that most fungal cells present in vessel lumina could be lost during sample manipulations. The advent of new techniques of tissue fixation and embedding made it possible to observe a greater number of pathogen elements that were not related to the inoculum. Yet, the first determinant of pathogenesis was not believed to be directly related to the sole physical detrimental effect of pathogen elements, so much so that their presence in paratracheal cells was only casually observed. Thus, investigations were carried out by other researchers to isolate possible toxins or hydrolyzing enzymes produced by the pathogen in order to determine if any of them could be related to the disease symptomatology, but still assuming that the dysfunction of vessel elements would be the main factor involved. In this scheme, the effect on paratracheal and adjoining cells would be one of secretion into vessel lumina of substances apt to favour or inhibit fungal growth, such as phytoalexins, or of compounds influencing host physiological functions or leading to anatomical changes such as tylose formation. Some of these substances were isolated and identified, but the presence of others was postulated rather than clearly ascertained. One issue in this respect was to determine beyond all doubt the origin and nature of the material deposited as lining on vessel walls. Yet, these factors were not always consistent between different hosts affected with similar diseases. In the course of our own transmission electron microscope and cytochemical studies of elms and non-hosts inoculated with the DED pathogen (conducted in collaboration with a number of people whose names appear as senior or as co-authors of some of the publications listed on the Web site) and of other plant wilt diseases, observations pointed to other possibilities that could explain the syndrome of these diseases, including host tissue alterations and reactions. Briefly, these studies showed that a large part of the substances that accumulate in vessel elements, including those forming linings, could be attributable to pathogen origin and be directly involved in tissue invasion and cell attacks. Pronounced breakdown of membranes of half- bordered pits and middle lamellae was also shown to be associated with the presence of unbound opaque matter, which was occasionally shown to pervade host secondary cell walls (particularly in young tissue) and reach into cell content. This matter was shown to label for DNA in elm and Fusarium-infected staghorn sumac (Rhus typhina L.). Visible cell reactions to such invasions included the deposition of new wall material in host cells, including fibres and vessel elements in some hosts, or the formation of compartmentalization tissues in elm trees (American elm, Ulmus americana L., and other species), in Fusarium-infected carnation …