PESTS AND DISEASES OF FORESTRY IN NEW ZEALAND
Pruning and cypress canker
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Formerly known as the Forest Research Institute, Scion has been a leader in research relating to forest health for over 50 years. The Rotorua-based Crown Research Institute continues to provide science that will protect all forests from damage caused by insect pests, pathogens and weeds. The information presented below arises from these research activities.
From Forest Health News 203, March 2010.
Cypress canker disease is one of the main reasons why cypresses, especially the popular but susceptible Cupressus macrocarpa, are not planted more widely on farms and in forests in New Zealand. This disease is caused by two species of microscopic fungi, Seiridium cupressi (previously known in New Zealand as S. unicorne) and S. cardinale.
These microfungi infect through natural wounds on branches and stems, and may also invade directly through younger shoots before secondary tissues are formed. But what about pruning wounds? Cypresses have many branches, some of which must be removed in order to produce quality timber and to reduce the risk of toppling and breakage in strong winds. It is therefore an important management question as to whether this operation leads to greater levels of disease. Could old pruning stubs at the centres of perennial stem cankers on more mature diseased trees have been the initial points of entry for the infection?
One earlier study found that pruning stress increased the severity but not the incidence of disease, but this was with the less susceptible C. lusitanica, and the question remains open for C. macrocarpa.
To address this question, two studies were undertaken two years apart in a young C. macrocarpa trial in the Scion grounds at Rotorua (cypress growers are understandably averse to researchers enthusiastically introducing the disease into their valuable plantations!). In the first study, when the stand was three years old, 275 trees were inoculated in approximately equal proportions with an isolate either of S. cupressi or of S. cardinale. Three branches were pruned on each tree and the fresh stubs were treated at the centre or the edge, the third wound being left untreated as a control. After one year, 75% of stubs inoculated at the edge, and 60% of those inoculated at the centre, became infected and produced stem cankers, whereas cankers were formed on only 2% of non-inoculated control stubs, the rest of which had healed naturally. There was a significant difference in incidence between the two isolates. This study proved unequivocally that both pathogens can invade through pruning wounds and cause disease.
But the experiment was artificial. What would happen if freshly cut wounds were simply left to become naturally infected? In the second study, two branches were removed on each of 161 trees during showery weather (asexual spores of the cypress canker pathogens are considered to spread in rain splash). One fresh stub was then bound with grafting tape (as was done with all stubs in the first study), while the other was left unbound. This time 11% of stubs gave rise to cankers, the remainder healing naturally. There was no significant difference in incidence of infection between bound and unbound stubs, and in both studies grafting tape made an imperfect seal. At least some of the natural infections were caused by S. cupressi, as shown by the production of fruit bodies of this species at the edge of a selection of the cankers.
In the second study a moderate level of infection was therefore induced simply as a result of pruning. Only two branches were pruned on each tree, so in a normal operation when many lower branches are removed, it is reasonable to assume that pruning will lead to some stem cankering if there is already a significant amount of disease present in the stand. Under the moist conditions that promote spore dissemination it seems unlikely that any increase in ventilation due to branch removal will discourage infection, especially in warmer regions where the disease is more severe.
Natural infection increased from 2% on uninoculated control stubs in the first study to 11% in the second experiment. The level of disease was low in the trial stand at the time of the first study but had increased substantially during the subsequent two years. The more than five-fold increase in natural infection between the two experiments is therefore explained by a greater incidence of background spore inoculum when the stand had become more heavily diseased. The results of this work thus indicate that rather than avoiding pruning when working with cypresses, especially C. macrocarpa, it is more important to maintain a low level of disease in a stand. Infected branches and whole trees should be removed and if possible destroyed as soon as symptoms appear, and there should desirably be no diseased cypress shelterbelts nearby. If this is not feasible, especially in regions where cypress canker is particularly prevalent, such as Auckland and Northland, it is better to consider planting a tree species not affected by the disease, at least until less susceptible C. macrocarpa cultivars are developed by forest geneticists and tree breeders. In addition, the results of these studies suggest that it may be useful to prune only during dry weather, and to clean or sterilise pruning tools between trees, for instance by washing in bleach or alcohol. However, the value of these practices still awaits experimental verification. The chief objective must be to maintain a low level of disease right from the start of a rotation.
The work in this article is reported in greater detail in: Hood, I.A.; Gardner, J.F.; Hood, R.J.; Smith, B.M.; Phillips, G.D. (2009): Pruning and cypress canker in New Zealand. Australasian Plant Pathology 38: 472-477. Copies of this paper can be obtained at www.australasianplantpathologysociety.org.au/
Ian Hood
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