Much has been said and written about the potential impact of the cinnamon fungus Phytophthora cinnamomi on native forests in parts of Australia. Particular attention has been focused on the jarrah forests of Western Australia, and their research provided a pace setter for the rest of Australia. It was also detected in some rain forests in Queensland, and the mixed eucalypt forests along the coastal regions of Victoria (especially east Gippsland). About 1000 ha of dieback and tree decline were observed in the coastal forests of east Gippsland in the 1950s, but the fungus was not isolated in these forests until 1969. Soon after (1970/71), acute dieback occurred over significant areas of these coastal forests (Marks and Idczak, 1977). As the type of injury sustained by trees varied considerably, it became evident at this time that, inter alia, disease expression depended on species, soil type, elevation and general climatic conditions. Exhaustive research followed the events of the 1960s and early 1970s.

Early assessments regarding the behaviour of P.cinnamomi and the nature of the disease were strongly influenced by research in horticultural crops carried out in the USA and Australia. With hindsight, it is now possible to say that this was not completely applicable to eucalypt forests in Australia. Subsequent research showed major differences existed so that forest managers are now in a far more comfortable position to assess the potential of the disease and to implement preventative and control strategies. Before considering the fungus in some detail, the origin of the pathogen warrants consideration as this has been the subject of protracted debate. As noted by Marks and Idczak (1977), there were two school's of thought on this matter in the early 1970s. One hypothesis considered that the fungus was introduced during early European colonisation and thence spread rapidly by agricultural practices, this being assisted by the wide range of suitable native hosts. The other hypothesis argued that the fungus invaded Victoria several tens of thousands of years ago. It is now generally accepted that P. cinnamomi is a newly introduced pathogen, and not a long time colonist or indigenous pathogen living in balance with the native flora (Marks, pers. comm.).

Initial research suggested that P. cinnamomi only attacked the unsuberised roots and severe "root pruning" eventually killed the trees by drought; species resistance varied and, as a rule, the Symphyomyrtus group were more resistant than the Monocalyptus. Early work demonstrated that unsuberised roots are readily penetrated by the fungus (via zoospores). Once established inside the roots, the fungus invades the cells intercellularly with occasional intracellular penetration. However, the fungus was isolated from the roots of a wide range of both tolerant and susceptible native plants which led to the belief that it had a wide host range, and the unproven suggestion that it was consequently very hazardous to Australian vegetation (on the assumption that root infection = tree death). But the precise mechanism for tree death remained obscure.

Distribution studies showed the fungus was present in soils over relatively large tracts of land throughout the State, yet tree damage continued to be confined to fairly well-defined areas. These enigma's remained unresolved in Western Australia and Victoria until about 1978.

From these initial studies, it became apparent that soil factors such as moisture and temperature status and microbiological properties were highly correlated with the pathogenicity of the fungus. The importance of soil type was clearly demonstrated by the work of Kassaby et al. (1977) who innoculated a fertile, well-drained mountain forest soil and found that the fungus did not infect undisturbed soil even after three years. Population levels of the original inoculum declined rapidly during this period. One conclusion reached from this work was that the fungus will have very little significance as a soil pathogen in such environments. While the reasons for this apparent immunity have not been positively identified, it is likely that the combined effects of a cool climate, well-drained soils and a rich soil microflora containing organisms antagonistic to P. cinnamomi are major contributing factors.

In recognition of the importance of soil type in disease expression in east Gippsland coastal forests, a study was commissioned by the Department. Results of this study were reported by Hough and Beams (1979) who found a strong relationship between dieback and topographic, soil and geological features. Dieback was most intense and extensive on soils derived from Tertiary sediments. Conversely, it was not recorded on reddish soils or on deep, freely draining sands. Dieback susceptible soils on the Tertiary sediments were generally characterised by slopes of less than 0.5° and a shallow (20 to 55cm) depth to an impeding, clay rich layer. This was particularly so in the Waygara Land System where severe and extensive dieback has occurred. This work therefore confirmed the role of soil type and topography in the destructive potential of P. cinnamomi.

Several unsatisfactory features were found in the "root pruning" hypothesis for tree death. Furthermore, P. cinnamomi appeared to behave differently in Western Australia and Victoria. Such a situation is biologically unacceptable. A major breakthrough in the understanding of the method by which P. cinnamomi kills eucalypts was made by Marks and Smith (1980). They produced evidence showing that the fungus can infect the stem and major roots of eucalypts. Furthermore, the fungus was able to persist in the stem for several months under field conditions, even in the lower elevation mountain forests. They also found considerable genetic variation in resistance to stem infection, and that some soils suppressed root infection while others assisted fungal invasion. Many soils such as krasnozems containing high levels of organic matter were disease suppressive. Conversely, the conducive soils were coarse, sandy and low in organic matter.

The final pieces of recent evidence that collectively clarify the role of P. cinnamomi in damaging our native forests relate to the stand development (or age), soil moisture status, genetic resistance and climatic factors. It has long been suspected that older trees have a greater sensitivity to the disease than younger trees. Smith and Marks (1982) present evidence to show that this could be due to a reduced ability of older trees to replace damaged roots. Following an indication from studies in Western Australia that certain wattles may produce toxins that afford protection to eucalypts, studies were initiated in Victoria. While no evidence of a toxin was found, the mortality rate of silvertop declined when wattle competed strongly for available soil water (Smith¹, pers. comm.). Furthermore, the rate at which infection spread within a eucalypt stem was many times slower under moisture stress. Thus moisture stress, contrary to all observations, increases disease resistance in eucalypts. This finding needs further testing because it has important silvicultural implications. The importance of soil moisture in disease expression was further demonstrated by a study of climatic conditions in south and east Gippsland from the 1880s to 1980 (Tregonning and Fagg 1982). They found that all dieback epidemics so far recorded in these regions occurred during years in which a 3 or 4 month period of high rainfall in the warmest months was immediately followed by a similar period of low rainfall. It is noteworthy here to mention that wet, warm soil is optimum for the propagation of the fungus. Finally, there is strong evidence of substantial genetic variation among a range of eucalypt species in disease resistance (Marks, pers. comm.).

Given all of the above evidence, it is clear that not only is the threat of P. cinnamomi considerably less than envisaged in the early 1970s, but also strategies for disease control developed on the basis of the fungus being a native organism that kills by root pruning alone need to be modified. A strategy currently being evaluated in east Gippsland relies heavily on the assumptions that disease expression is reduced by decreasing the amount of available water in the surface soil horizons, that some eucalypt species are far more resistant to the disease than other species, and that there is significant genetic variation within a species in disease resistance. The strategy incorporates a conservation and regeneration component. The former consists of a moratorium on felling disease-resistant eucalypt species in order to conserve these seed sources, and a ban on so-called selective cutting. The regeneration component first requires a knowledge of the original (prior to selective cutting) species distribution, an estimate of the disease hazard of the site, and the amount of disease present before the site is clearfelled and the slash burnt. The site is then sown, with a seed mixture approximating the original species composition, at heavy rates to ensure dense regeneration that will maximise water use and aid in selection for resistance amongst susceptible species in the mix. It will be several years before the effectiveness of this strategy can be fully evaluated. In the meantime, the important elements of the strategy are being incorporated into existing silvicultural systems for east Gipppsland.

Because P. cinnamomi also attacks and kills a few species of native wildflowers and woody shrubs, care must be taken in reserves and parks to prevent or minimise its spread by implementing appropriate quarantine procedures. Such measures are used as needed.

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