MSU Extension

Editor’s note: This article is from the archives of the MSU Crop Advisory Team Alerts. Check the label of any pesticide referenced to ensure your use is included.

MSU Diagnostic Services and several professors, campus arborists and others have had quite a struggle with diagnosing the cause of the many mysterious problems in maples that have appeared this year. Maples are not the only trees we are encountering with such problems though. Equally mysterious samples of damaged or dead spruce and oak have arrived for diagnosis. While we remain baffled by the lack of any pathogen or pest associated with the trees, I would propose to you that the cause for the tree problems may have occurred during the winter and left no visible trace in the trees. It will take some sophisticated work to support the ideas I present here and with the autumn approaching our time to test the hypothesis may have passed; therefore, this diagnosis will likely remain speculative, unfortunately.

There has been a long history in forestry of pathologists struggling with the causes of forest declines, and it is in this literature that we may encounter some answers to the maple problems. Maples and particularly sugar maples have shown recurring episodes of decline in forests which have been discussed since the 1940s. The causes of decline in sugar maple, oak and other species have been slowly worked over by studying associations of tree rings with climate and insect or fungal defoliators. Briefly stated (a difficult task for any old professor to do!), years of speculations and correlations have arrived at an understanding that defoliators, drought, root freezing, and root thaw-freeze cycles lead to individual trees declining and even dying. The most obvious symptoms expressed by affected trees include marked deterioration of the crown health. We do not appear to have a serious defoliator affecting the urban tree samples, so we must look to the other stressors for the hypothesis. However, in the forests in some parts of the state the forest tent caterpillar is doing serious damage that will likely result in some stress-induced mortality next year.

Stressed trees die slowly in many sites and situations. Studies have shown that trees exposed to severe drought generally separate into two classes in subsequent years, those that recover and those that begin to show decline in the crown health and reduced growth (basal area increment, BAI). This grouping of trees remains evident for many years and when a later moderate to severe drought episode occurs, the “declined” trees fail to recover when climate improves. They may show a steady state condition or exhibit a continued downward trend in health. The growth rate of these trees also can be profoundly affected by mild, short-term droughts.

From the standpoint of our large older landscape and forest trees, the severe drought of 1988 may still be taking a toll on their health and mild drought can have profound effects on them; drought where several months occur with less precipitation than historic averages. I believe that the more recent drought stress of the 2007 growing season may have triggered recent declines and mortality in this predisposed set of the “declined” trees. For the declining and dying maple and oak trees that have been sent to MSU for diagnosis, those reported to have begun showing scorched foliage and branch dieback the year or two years previously, I believe they are the “declined” set slowly exhibiting the effects of the 2007 drought (and root freeze, see below).

It is a hard concept for us to accept that long past stresses can kill trees without the additional attack by opportunistic pathogens or pests such as Armillaria root rot or bark beetles. However, we have been forced into speculating along the above theme because few of the dying maples and other trees showing damage this year have exhibited Armillaria root rot. Of course, some have, and when tree rings were examined in the Armillaria infected trees, it was evident that incremental growth had been greatly reduced for several years, not just this year. These trees all exhibited scorch-like symptoms on the leaves and dieback of the terminal tips of branches (new growth), and sometimes whole branch death, or entire tree death.

It is less hard to conceive of a single stress event causing dieback and death of trees, unless that single event occurred disjointed in time from the symptom expression. The thaw-freeze events of this past winter are just such an overlooked and somewhat forgotten event that would have taken a toll on tree health and initiated decline. The winter before, I believe also had an unusual number of thaw-freeze events that would have damaged roots. Root freezing may have been evident in some large scorched and dying oak trees we examined where the roots looked as though they had been dead for many months yet did not have Armillaria root rot. In addition to the harsh thaw-freeze cycles of our recent winters and the documented effects of similar climate on forest sugar maple declines, this winter one of our thaw episodes was followed by an evening extreme drop of 30°F to record cold January temperatures. This particular freeze spell may be our primary causal agent in the maple scorch, dieback, and mortality that is so unusual and widespread this year. Maples have been experimentally shown to suffer greatly from such root freezes. Perhaps in those maples affected this year, the roots were in a shallow or other position conducive to freezing more so than unaffected trees of the same species or other species in the region.

One major after-effect of root freezing and the extreme cold drop in January was likely cavitations in the vascular system, the disruption of the water columns by ice formation. The breaking of the water capillaries by ice formation introduces air-pockets that disrupt the water flow in the trees. This disruption may not be repairable by the maple species during spring growth. The expected effects of cavitations would be similar to several of the symptoms that have been present in our damaged maples, including: leaf scorch, leaf drying and curling, shriveling of the terminal new twig growth, eventual branch dieback, and even tree death. Cavitations are essentially invisible under ordinary examination of plants during diagnostics. So ascribing blame to this mechanism comes about from the absence of other evident causes, for example, Verticillium wilt. None of the samples of maple scorch and branch dieback that I have examined yielded Verticillium during isolations. This has been an unexpected finding all year for the damaged maples, because stresses such as drought, almost always lead to increased incidences of Verticillium infection of maples, red buds, smoke trees and viburnums. Verticillium wilt also results in scorch-like leaf symptoms, branch dieback and occasionally tree death and these were the symptoms we were regularly seeing in diagnostic samples and in the field, yet lab tests showed the Verticillium wilt pathogen to be absent.

In conclusion, the hypothesis that root freezing, thaw-freeze cycles, and past drought stresses have resulted in trees exhibiting severe decline, dieback and even death seem to be supported by the symptoms expressed in maples and other species. In urban maples in particular, cavitations in the vascular system caused by the January thaw-extreme freeze episode seems a probable cause of the symptoms we are witnessing. However, as we university folk are famous for saying, more research is needed to verify our best assumptions.