3.7.4S
CRYPHONECTRIA CANKER OF EUCALYPTUS

MJ WINGFIELD and BD WINGFIELD

Tree Pathology Co-operative Programme, Forestry and Agricultural Biotechnology Institute (FABI), University of Pretoria, Pretoria 0002, South Africa

Background and objectives
Approximately eight million hectares of Eucalyptus are currently propagated in intensively managed plantations in various parts of the world. The current trend is to propagate Eucalyptus species vegetatively, which also allows the large scale deployment of hybrids. This has led to the establishment of plantations, with a relatively uniform genetic base. The risks due to disease are substantially enhanced, and severe losses have already been experienced.

Cryphonectria cubensis is one of the most serious canker pathogens of Eucalyptus in the tropics and sub-tropics [1]. Losses in seedling stands, have led to the introduction of vegetative propagation, and the deployment of disease tolerant hybrids. Using this approach, the impact of cryphonectria canker has been substantially reduced. However, selection of disease tolerant planting stock is generally based on field observations. Very little is known about the pathogen, its origin, genetic diversity or its capacity to overcome disease tolerance in selected clones. The aim of this report is to briefly review studies aimed at reducing the impact of cryponectria canker, particularly in South Africa, but also elsewhere.

Results and conclusions
Cryphonectria cubensis is thought the be synonymous with the clove pathogen Endothia eugeniae. The fungus might thus have originated on clove, which is native to Indonesia [2]. Our recent studies based on RDNA sequence data have confirmed the similarity between C. cubensis and E. eugeniae and also that the fungus is present in Western Australia. The fungus is also present on native plants in South America. Studies of the genetic diversity of C. cubensis populations suggest that the pathogen is genetically diverse and well established in South America and Indonesia, where sexual reproduction in the pathogen is also common. In contrast, the pathogen has a limited genetic diversity and reproduces only asexually in South Africa (see contributed presentation by Van Heerden et al.). Cryphonectria cubensis isolates in South Africa appear to be more closely related to South American than South East Asian isolates. The likely origin of the pathogen remains obscure, with potentially native hosts known in Australia, South East Asia as well as South America.

Symptoms of crypohonectria canker in South Africa are somewhat different to those in other parts of the world, which is intriguing. Inoculation studies in South Africa, Indonesia and South America also suggest that the South African isolates of C. cubensis have a different biology to those from the other countries. In South Africa, inoculation of clones gives a clear view of their relative susceptibility, prior to commercial deployment. This is a useful tool for forest managers and it is now being evaluated in Indonesia and various South American countries. Through artificial inoculation, eucalypt genotypes representing a range of tolerance to C. cubensis have been identified and introduced into breeding studies. The resultant parents and progeny are now being used to develop rapid DNA-based screening techniques.

Although it is not viewed as an alternative to breeding and selection of disease tolerant clones, biological control of C. cubensis through dsRNA mediated hypovirulence could be useful. This would especially be true in countries such as South Africa where C. cubensis appears to be recently introduced and represented by a limited genetic diversity. dsRNA has recently been discovered in South African and Brazilian isolates of C. cubensis and is currently being studied. The potential to utilise C. cubensis isolates transfected and/or transformed with ds RNA from Cryphonectria parasitica, is also being considered.

References
1 . Conradie E, Swart WJ , Wingfield MJ, 1990. South African Forestry Journal 152, 43-49.
2. Hodges CS, Alfenas AC, Ferreira FA, 1986. Mycologia 78, 334-350.