Pathologists disagree about what, if anything, constitutes a decline disease (hereafter “decline”), and if you consider other scientists who concern themselves with tree mortality, the term is used even more generically. Some use the term for:
- damage for which the cause is not known, or
- any episode of widespread branch dieback and mortality, or
- damage where more than one agent can be involved.
None of these meet the criteria of thinkers who have advanced decline concepts.
I once was a professor at the College of Environmental Science and Forestry in Syracuse with Dr. Paul Manion, one of the foremost proponents of decline concepts [6, 7, 10, 11]. On probably too many occasions, I put forward my thinking that a decline concept was unnecessary and that it is already addressed by a robust, flexible concept of disease and the disease triangle. This opinion has been laid out more recently by others in a publication .
My view changed when I worked on a decline myself – sudden aspen decline. After gaining an understanding of the various categories of causal factors and sequences, I began to see the utility of the decline concept—perhaps not strictly necessary, but useful. A tip of the hat to Paul.
The greatest utility is communication. One can lay out a series and sequence of important causal factors, give it a label, and help people understand there are multiple causes. Yes, a typical disease carries the same complexity, but let’s face it, people tend to focus on the pathogen. Even some pathologists equate disease and pathogen in their writing 😟. And if there is no primary biotic pathogen, which is usually the case with decline diseases, people will simply call it drought mortality or similar, which is just as oversimplified.
Once it is called drought mortality, all the other causal factors will be ignored by everyone but the pathologists. They may be ignored anyway, but at least, as a decline disease, we have a better chance to raise awareness of the other causes. As it is, it seems most ecologists who study drought-associated mortality believe drought causes direct, physiological mortality, and largely ignore the biotic agents that often, if not usually, do the actual killing. This is important, because it is quite possible that many trees would recover from the drought, if not for the biotic agents that hit them when they are weak.
Several reviews have been published on decline diseases. Sinclair and Hudler wrote a concise, no-nonsense review summarizing and comparing the concepts to date , and Sinclair updated the discussion in his monumental tome, Diseases of Trees and Shrubs . A review in 1989 focused on declines of hardwoods in the eastern USA . Many of the decline concepts are presented by their original authors in the symposium publication, Forest Decline Concepts . Finally, a truly global overview of declines is presented by Ciesla and Donaubauer . That publication includes information on declines in various parts of the world for which little or nothing else is published.
Symptoms of decline diseases vary with the specific causes, but can include :
- slow growth
- sparse, small, often chlorotic foliage
- premature autumn color
- premature leaf drop or poor needle retention
- distress crops of fruit
- reduced storage of food reserves
- dieback of twigs and branches
- adventitious sprouts following branch dieback
So without further ado, let’s explore decline concepts.
Multiple Decline Concepts
Sinclair’s concept of decline is probably the most versatile and adaptable to various situations, because it is really multiple concepts [14–17]. By acknowledging that decline diseases vary in the types and sequences of causal factors, he avoids forcing all declines to fit a single pattern. He defines decline as premature, progressive loss of vitality due to stressing factors over a period of years. Normal senescence of aged trees is excluded because most trees, if they survive long enough, inevitably pass through a phase of reduced growth and senescence before death.
Sinclair presents four models that accommodate most declines:
- Decline caused primarily by continued/chronic stress by one factor. These might be phytoplasmas, viruses, and some slow-acting parasites of foliage, roots, or sapwood. Apparently this model merits recognition as decline diseases only because of the slow action.
- Decline caused by drastic injury plus secondary stress. A major, short-term event such as severe drought, storm damage, or insect defoliation reduces vitality such that opportunistic pathogens and insects can invade. They prevent recovery and indeed ratchet down the health of the tree over time. Neither of the two factors would cause decline alone.
- Decline caused by interchangeable predisposing, inciting, and contributing factors. This concept, first proposed by Sinclair in 1965 , was later popularized and developed by Manion (see below). Sinclair’s original concept is less restrictive than Manion’s about the types and severity of agents that can fill the three roles.
- Predisposing factors. These are often edaphic factors. They reduce the ability of trees to withstand injury or biotic attack.
- Inciting factors. These are usually events, such as drought or defoliation, rather than chronic conditions. They result in the first symptoms of decline and reduced ability to tolerate adversity.
- Contributing factors. The above agents plus a variety of insects and pathogens can contribute to decline, once incited. They include further defoliation by insects or frost, adverse soil conditions, and a wide variety of secondary insects and pathogens.
- Cohort senescence. This matches the concept proposed by Mueller-Dombois, which essentially states that a group of trees of the same approximate age will reach an aggregate biomass that cannot be sustained by a given site, and senesce at about the same time. Sinclair & Hudler  noted that this concept is really a version of the previous one, with tree age as a predisposing factor.
Sinclair presents some interesting propositions, which could be considered principles, useful in understanding decline diseases . Among them are:
- Tree growth and development vary widely from site to site and may fluctuate widely on a given site, yet still be judged normal.
- Trees growing in constructed sites and in disturbed forest sites are stressed by factors not encountered by trees in undisturbed forests.
- Individual trees vary in exposure and responses to stressing factors.
- A change in intensity or supply of an environmental factor may cause stress.
- A factor that is harmless after short exposure may, if applied chronically, predispose trees to damage by other factors or may cause damage directly.
- Accumulated stress results in inability to respond to favorable conditions, but also inability to tolerate or resist the unfavorable ones.
- Repetitive minor injuries or stress may have cumulative effects.
- A factor that triggers decline may cease causing stress, but secondary or contributing factors may perpetuate stress and cause decline.
- Old trees are less resilient than young ones.
Stress + Pathogen = Decline
This is the essence of Houston’s decline concept [2–5], in which disease is caused by two groups of factors. An adverse environmental factor, or stress, leads to often lethal attacks by secondary-action organisms that are otherwise insignificant . He refers to “dieback and decline diseases”. Apparently the terms are considered synoymous when used to name diseases, but are also used to refer to symptoms, branch dieback occurring first and followed by further dieback, growth loss, and loss of vitality referred to as decline. Branch dieback may begin even with the initial stress alone [2, 3]. The secondary organisms generally cause the decline phase, often leading to mortality.
The simplicity of this concept highlights a drawback that can apply to the concept of decline diseases in general . Where do we draw the line between a dieback/decline disease and diseases ordinarily not considered as such? A great many diseases, such as many Cytospora cankers, depend on prior stress by drought or other factors for infection and invasion. Should we consider them all decline diseases?
In some cases, different phenomena are lumped under the same name. For example, ash dieback was initially considered to be caused by the stress of drought, followed by attack by at least two opportunistic canker fungi that normally colonize senescing lower branches, Cytophoma pruinosa and Fusicoccum sp. Later, branch dieback and sometimes mortality were found to be caused by severe infections of ash rust, and the opportunistic canker fungi were not involved, but it is still “ash dieback” . Similarly ash yellows causes branch dieback and other symptoms and is considered yet another stress leading to “ash dieback”. With so much included in the characterization of the disease “ash dieback”, the disease name and decline concept become less useful.
In a paper focused on urban forests , Houston makes a point that managers of developed landscapes should take to heart: although the secondary organisms/facultative parasites often assume greater importance in urban environments under stress than in natural habitats, control of such dieback-decline diseases usually requires preventing or reducing the effects of the stress agents, rather than controlling the secondary-action organisms that cause mortality.
The Decline Spiral
Manion further interpreted and popularized Sinclair’s third model, interchangeable predisposing, inciting, and contributing factors [6–8, 10]. In this view, at least three factors must be involved in a decline, at least one from each of the categories. Manion broadened the concept of predisposition to include age, genetics, and virus infection.
The presentation of this model as a chapter in Manion’s textbook  raised the profile of decline diseases among forest scientists. The visual portrayal of the progress of decline as a spiral obstacle course also helped popularize the concept. Predisposing, inciting, and contributing factors each nudge the tree inward to the next level, with the center of the spiral representing death. If a subsequent factor type does not occur, the tree may presumable climb back to the outer ring. One can’t help but imagine a toilet bowl being flushed in slow motion, with the tree as a bug trying to swim out of the vortex.
Manion distinguished between decline disease, simply a type of disease, and forest decline, where whole forests are affected by decline. He also made the point that little progress will be made in understanding unnatural forest decline until natural diseases, including decline, were well understood and recognized.
Manion emphasized that death of trees and even large numbers of trees may be normal; the natural progression of forest dynamics . Similarly, he posited that in forests there was a “healthy amount of disease” that contributed to thinning as stands develop, and that even when mortality in one species exceeded that level, another species generally gained in the process of succession [8, 9].
- 1.Ciesla WM, Donaubauer E. 1994. Decline and Dieback of Trees and Forests: A Global Overview., Vol. 120 FAO Forestry Paper vol. Rome: Food and Agriculture Organization of the United Nations <https://books.google.com/books?hl=en&lr=&id=FDgYfi1G8L0C&oi=fnd&pg=PR1&ots=LuEuNfGp-f&sig=FCsakLKPn8LdytRetlkSzeZseno#v=onepage&q&f=false>.
- 2.Houston DR. 1981. Stress Triggered Tree Diseases: The Diebacks and Declines. NE-INF-41-81. Broomall, Pennsylvania: USDA Forest Service, Northeastern Forest Experiment Station.
- 3.Houston DR. 1984. Stress related to diseases. Arboric J 8(2):137–149 <http://dx.doi.org/10.1080/03071375.1984.9746670>.
- 4.Houston DR. 1987. Forest tree declines of past and present: current understanding. Can J Plant Pathol 9(4):349–360 <http://www.tandfonline.com/doi/abs/10.1080/07060668709501868>.
- 5.Houston DR. 1992. A host-stress-saprogen model for forest dieback-decline diseases. In: Forest Decline Concepts, eds Manion PD, Lachance D, pp. 3–25. St. Paul, Minnesota: American Phytopathological Society.
- 6.Manion PD. 1987. Decline as a phenomenon in forests: pathological and ecological considerations. In: Effects of Atmospheric Pollutants on Forests, Wetlands and Agricultural Ecosystems. NATO ASI Series (Series G: Ecological Sciences), vol. 16, eds Hutchinson TC, Meema KM, pp. 267–275. Berlin, Heidelberg: Springer.
- 7.Manion PD. 1991. Tree Disease Concepts. Englewood Cliffs, New Jersey: Prentice-Hall.
- 8.Manion PD. 2003. Evolution of concepts in forest pathology. Phytopathology 93(8):1052–1055 <10.1094/PHYTO.2003.93.8.1052>.
- 9.Manion PD, Griffin DH. 2001. Large landscape scale analysis of tree death in the Adirondack Park, New York. For Sci 47(4):542–549 <10.1093/forestscience/47.4.542>.
- 10.Manion PD, LaChance D. 1992. Forest decline concepts: An overview. In: Forest Decline Concepts, eds Manion PD, LaChance D, pp. 181–190. St. Paul, Minnesota: American Phytopathological Society.
- 11.Manion PD, LaChance D, eds. 1992. Forest Decline Concepts. St. Paul, Minnesota: APS Press. 249 pp.
- 12.Millers I, Shriner DS, Rizzo D. 1989. History of hardwood decline in the eastern United States. General Technical Report NE-126. Broomall, Pennsylvania, USA: US Department of Agriculture, Forest Service, Northeastern Forest Experiment Station <https://www.fs.usda.gov/treesearch/pubs/4177>.
- 13.Ostry M, Venette R, Juzwik J. 2011. Decline as a disease category: Is it helpful? Phytopathology 101(4):404–409 <10.1094/PHYTO-06-10-0153>.
- 14.Sinclair WA. 1965. Comparisons of recent declines of white ash, oaks, and sugar maple in northeastern woodlands. Cornell Plantations 20(4):62–67 <https://forestpathology.org/pdfs/sinclair1965_comparisons_of_declines.pdf>.
- 15.Sinclair WA. 1967. Decline of hardwoods: possible causes. Proceedings of the International Shade Tree Conference, 1966 42:17–32 <https://forestpathology.org/pdfs/sinclair_1967_decline_of_hardwoods.pdf>.
- 16.Sinclair WA, Hudler GW. 1988. Tree declines: Four concepts of causality. J Arboric 14(2):29–35 <http://joa.isa-arbor.com/articles.asp?JournalID=1&VolumeID=14&IssueID=2>.
- 17.Sinclair WA, Lyon HH. 2005. Diseases of Trees and Shrubs. Ithaca, New York: Cornell University Press. 660 pp. 2nd ed.