Bio of Forest Steward

May 14, 2010

Sudden (10 years, anyway) Oak Death marches on

Article reviewed:  Responses of oaks and tanoaks to the sudden oak death pathogen after 8 years of monitoring in two coastal California forests

By B.A. McPherson, S.R. Mori, D.L. Wood, M. Kelly, A.J. Storer, P. Svihra, and R.B. Standiford, published in Forest Ecology and Management 2010 Vol 259 pp 2248-2255

The plot line: The researchers closely monitored the progression of Sudden Oak Death (SOD) over 8 years, tracking the rate of mortality in coast live oaks, California black oaks, and tanoaks. They compared SOD-caused mortality with mortality not related to SOD (i.e., the “background level” of mortality). Over the monitoring period, they observed a steady increase in SOD infections (bad news for oaks) coupled with a steady decrease in trees without SOD infections (also bad news for oaks). It was much more common for trees to die from SOD infections than for reasons not related to SOD, by a factor of 7 to 9 (very bad news for oaks).  

Relevant quote: “Under the pressure of this aggressive pathogen, the presence and propagation of resistant genotypes among the host oaks and tanoaks may provide the best chance for sustainable wildland populations of these species and for management of these forests.”

Relevance to landowners and stakeholders:

When SOD was first identified as the cause of widespread oak mortality in 2000, there was a huge amount of attention drawn to it. Whoever gave it the name “Sudden Oak Death” was a genius if they were trying to draw media attention to the disease. In addition to the name being inherently catchy, “Sudden Infant Death” was in the news at the same time so SOD got some bonus hype via phonetic-association. The disease deserved the attention it received (although I wonder what kind of attention and funding it would have received had it occurred somewhere other than coastal California). At the time, scientists and managers were wondering if SOD would march through all of the western US, leaving billions of dead trees in its destructive path.    

Permanent monitoring plots that are revisited year after year are a good way (perhaps the best way) of tracking how forests change. It appears that the range of the SOD impact on native forests has not expanded in the last decade, but the disease continues to have a profound influence on the forests where it has been established (central and northern coastal forests of California). Mature tanoak, California black oak, and coast live oak trees are dieing at a much faster rate than they otherwise would. If the mature trees are not replaced with resistant trees, the decline of these species’ populations in SOD-impacted areas will continue.  

Relevance to managers:

The relevant metric in this case is the comparison of SOD-caused mortality rate to background mortality rate. The SOD-caused mortality rate for live oak was 3.1% per year. It was 5.4% per year for tanoak. This may not sound like a lot, but it is indeed a very high mortality rate, especially when compared against the background rate of 0.33% per year for live oak and 0.75% per year for tanoak.

Besides the relevant quote given above, no explicit relevance is provided for managers in this paper. My inference is that this paper provides documentation that SOD-related mortality rates continue to be very high and that managers should be anticipating very significant change in SOD-affected forests. Managers should expect species composition shifts, and therefore shifts in processes such as nutrient cycling and fire behavior as well.

As was the case when this disease was first discovered, a lot of attention and funding is still being given to SOD research and outreach programs. More information is available at here.

Critique and/or limitations (there’s always something, no matter how good the article is) for the pedants:

For an article in Forest Ecology and Management, it has very little content in terms of explicit management implications. The one sentence referring to management suggests that propagation of resistant genotypes could be a worthwhile management response. This idea could have been developed more. How much do we know about current levels of resistance? Are there resistant breeding programs in place? Not that it couldn’t be done, but it would seem to take a lot of work to create an operational nursery program and infrastructure for oak species that currently are not widely planted.

It was unclear to me whether or not IN-GROWTH was measured in these plots. If it was just tracking individual trees over time without also tracking in-growth of new trees, then we are only getting one side of the equation in terms of knowing long-term population trends. I am assuming that in-growth was indeed measured, but the authors did not explicitly say that this was the case so I’m not sure.

It also would have been very helpful to report the overall change in basal area over time. Given the rapid mortality rates and the fact that mature trees are infected readily, I would expect that basal area declined substantially over the monitoring period. Knowing the change in basal area over time gives more information about how competition-related stand dynamics might be interacting with the pathogen. Since they did not report change in basal area, it makes me think that perhaps in-growth was not measured?