The impact of a canker disease of Corymbia calophylla (marri) in the southwest of Western Australia (WA) has increased substantially since it was first observed causing decline and death of this species in the 1970s. By the early 1990s there were expressions of concern and calls to determine the cause and management options. Despite this, there has been very little research into the incidence, severity and possible causes of the disease. There are, however, historical reports dating back to the 1920s of a canker disease of amenity planted C. ficifolia caused by Sporotrichum destructor, though the diagnosis and Latin description were never published. It has been suggested that there may be links between this species and the genus Quambalaria, a group containing leaf and shoot pathogens of species of Eucalyptus and Corymbia. This study examined the incidence and symptomology of the disease, the range of fungal species associated with healthy and diseased C. calophylla, and the pathogenicity of isolates obtained from these surveys. Also investigated was the identity of the pathogen, S. destructor, historically attributed to canker disease of C. ficifolia, to determine whether this pathogen is responsible for the current epidemic of C. calophylla canker and if it is synonymous with Quambalaria. Cankers were present on trees across the range of surveyed sites, with lesions occurring on trunks, branches or twigs of 25.7 % of the C. calophylla surveyed. Canker incidence was significantly greater on trees present at remnant sites, such as roadsides and in paddocks, than forest trees being 38 % and 13.3 %, respectively. Tree height, trunk diameter at breast height and crown position, size and health ratings were significant predictors of canker presence, with cankers more common on larger, older trees and trees with poor crown condition. Bark cracks exuding kino were present on 48 % of the surveyed trees, and when dissected, lesions were observed on 40 %, suggesting that these cracks could be the initial stages of canker disease. This was confirmed by the observation of a number of cracks that developed into perennial cankers during the three year study. Monitoring of canker development and the examination of transverse sections showed the circumvention of host defenses by the pathogen and the subsequential walling off response of the host (which typifies perennial cankers) was not necessarily an annual event, with no change observed in some cankers over the three year period, while others progressed rapidly in that time, occasionally to the point of girdling and killing the host. Initial surveys isolated 44 fungal species from healthy and diseased C. calophylla, with opportunistic pathogens including Endothiella eucalypti and Cytospora eucalypticola common. Subsequent surveys foccussed more on a potential pathogen in the genus Quambalaria, which was rarely isolated from active lesions, presumably because of its slow growth rate, but which sporulated consistently on the surface of older sections of the cankers. DNA sequences confirmed that Q. cyanescens and Q. pitereka are present in southwest WA, with the latter associated with leaf and shoot disease. A third and new species of Quambalaria was isolated from cankers. Comparisons of disease symptoms and conidiogenesis indicate this species is synonymous with S. destructor. The species is formally described here as Q. coyrecup T. Paap sp. nov. A pathogenicity trial was unsuccessful in causing disease symptoms in trees inoculated with core plugs taken from canker lesion margins of diseased trees, though the time frame and environmental factors may not have been adequate for disease development. The core plug inoculation method may also have failed because opportunistic pathogens which were frequently isolated from lesions out-competed Q. coyrecup (paralleling the results achieved by culturing from lesions). Quambalaria coyrecup caused symptoms matching those observed in natural infections when suitable hosts were inoculated, confirming it is the fungus responsible for the current canker disease of C. calophylla and C. ficifolia. Endothiella eucalypti also caused significant lesions, though these were not typical of natural infections, which together with its frequent isolation from both healthy and diseased trees suggests it is an opportunistic pathogen, potentially contributing to disease development in trees already infected with Q. coyrecup. Isolates of Q. pitereka from WA and eastern Australia both caused typical shoot blight symptoms in the WA hosts C. calophylla and C. ficifolia, and the eastern Australian host C. maculata, though a larger path trial is required to examine the possibility of host specificity. Quambalaria cyanescens was non-pathogenic in all inoculation trials. The current cause of cankers in C. calophylla is now known to be the same as the fungus historically implicated in the canker disease of C. ficifolia, when at the time it was described as an endophyte doing little or no damage in C. calophylla. Thus, it is of immediate importance to determine the factors driving this decline, and develop control and management options.